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Volume 36,2026 Issue 2

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Research Progress on the Mechanism of Traditional Chinese Medicine in Improving Diminished Ovarian Reserve Function by Regulating the PI3K/AKT Signaling Pathway

dingwenjia

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Diminished Ovarian Reserve (DOR) refers to a complex gynecological disorder characterized by reduced quantity and impaired quality of oocytes in the ovaries. It affects millions of women worldwide, often leading to menstrual irregularities and infertility. With the delayed age of marriage and childbearing, DOR has become a key factor impacting women's fertility.This article summarizes the multiple pathogenic mechanisms and signaling pathways involved in the occurrence and development of DOR, among which the Phosphatidylinositol 3-Kinase/Protein Kinase B (PI3K/AKT) signaling pathway plays a core role in the regulation of ovarian function. The article demonstrates that the PI3K/AKT pathway exerts a significant effect on the pathogenesis of DOR: it influences the occurrence and progression of DOR by regulating granulosa cell apoptosis, modulating ovarian inflammatory responses, and governing the autophagy and oxidative stress processes of granulosa cells and follicular cells.Furthermore, this article focuses on summarizing the close association between the PI3K/AKT pathway and the pathogenic mechanism of DOR, as well as reviewing the latest experimental studies on the treatment of DOR using traditional Chinese medicine (TCM) monomers and compound prescriptions via this pathway, thereby providing references for the further advancement of DOR treatment research.
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A basic study on the delay of lumbar intervertebral disc degeneration by traditional Chinese medicine based on ferroptosis theory

CHEN CHAO QI

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Ferroptosis is an iron-dependent form of programmed cell death and plays a key role in the pathological process of lumbar disc degeneration (IVDD). Traditional Chinese medicine, with its advantages in overall conditioning, has demonstrated unique potential in the prevention and treatment of IVDD. This article starts from the pathological mechanism of IVDD and its interaction with ferroptosis, revealing that ferroptosis is not only a pathological driving factor but also a therapeutic regulatory target.. The theory of ferroptosis has great potential in guiding the intervention of IVDD with traditional Chinese medicine. By targeting the key pathways of ferroptosis and exploring the potential mechanisms of ferroptosis-related genes, it provides a new perspective and theoretical basis for the prevention and treatment of IVDD with traditional Chinese medicine, and also lays the foundation for the development of precise treatment strategies.
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Research progress on intervention Strategies for the Blood-Brain Barrier

maoxuqing, chenting, zhangshanshan

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【】: The blood-brain barrier (BBB) is a dynamic interface for selective molecular trafficking between blood and brain parenchyma, playing a pivotal role in maintaining central nervous system (CNS) homeostasis. Recent investigations have uncovered intricate regulatory networks governing BBB function, involving dynamic [1]remodeling of intercellular tight junctions, activation of signaling cascades, and multicomponent interactions within the neurovascular unit.This review systematically synthesizes current mechanistic insights into BBB regulation.Moreover, it also focuses on pathological remodeling observed in various neurological diseases. Emerging interventional strategies, including nanotechnology-based drug delivery systems, gene editing, and traditional Chinese medicine (TCM) formula interventions, are critically evaluated with emphasis on their translational potential. By integrating bench-to-bedside perspectives, this work aims to provide novel theoretical frameworks for developing precision therapies targeting BBB dysfunction in neurological disorders.
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eviates post-stroke depression through regulating neurobiology

Xian Rong, Yang Zhipeng, Wang Tian, Wang Chao, Lin Zhengyu, Liu Haijing

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Post-stroke depression is the most common mental complication after stroke, seriously affecting the recovery of neurological function and quality of life of patients. Although antidepressants are currently the first-line treatment, they have limitations such as cardiotoxicity, gastrointestinal reactions and relatively high cost. Auricular therapy, as a non-pharmaceutical intervention method integrating traditional Chinese medicine and modern neuroanatomy, has shown unique advantages in the treatment of PSD through a multi-target regulatory mechanism. From the perspective of neurobiology, this article systematically reviews the mechanism of auricular therapy in the intervention of PSD, mainly including: (1) Regulating the homeostasis of monoamine and amino acid neurotransmitters; (2) Promote neural plasticity and the reorganization of brain network functions; (3) Inhibit neuroinflammation and oxidative stress responses; (4) Regulate the neuroendocrine system. The aim is to comprehensively explain the mechanism by which auricular therapy alleviates PSD through a multi-dimensional regulatory network of "neuro-immune-endocrine", and topromote further research and application of auricular therapy in the treatment of post-stroke depression.
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The Role of SREBP in Metabolic Dysfunction-Associated Steatotic Liver Disease and Its Targeted Interventions

chengcongcong, kangchenyang, wangyayuan, chenli

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Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) represents a global health issue characterized by excessive hepatic lipid accumulation, insulin resistance, and oxidative stress. Sterol Regulatory Element-Binding Proteins (SREBPs), particularly SREBP-1c and SREBP-2, are key transcriptional regulators of lipid synthesis and cholesterol metabolism. Growing evidence indicates that SREBPs play a central role in the pathogenesis of MASLD by modulating lipogenesis, interacting with insulin signaling pathways, and regulating endoplasmic reticulum stress and oxidative stress. This review explores the role of SREBPs in the pathogenesis of MASLD, along with related influencing factors and therapeutic strategies, providing valuable insights for a deeper understanding of the disease mechanisms and for the development of novel SREBP-targeted treatments.
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Research Advances on Acid-Sensing Ion Channel 1a (ASIC1a) in Drug Abuse

PU Shan, XU Ruike, LI Yunlan, LI Lihua, YANG Genmeng, HONG Shijun

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Acid-sensing ion channel 1a (ASIC1a), a proton-gated cation channel widely expressed in the central nervous system, is involved in various physiological and pathological processes by regulating calcium and sodium influx, synaptic plasticity, and reward effects. Recent studies have demonstrated that ASIC1a plays a pivotal role in drug abuse. By modulating neuronal excitability, synaptic plasticity, and reward circuitry, ASIC1a has emerged as a key molecule in research on the mechanisms of drug addiction and a potential therapeutic target. This review systematically summarizes the molecular characteristics of ASIC1a, its neuroregulatory mechanisms, and its regulatory role in drug abuse, aiming to provide novel targets for elucidating the mechanisms of drug addiction and to explore new strategies for addiction withdrawal therapy.
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Research Progress on the Vagus Nerve-Mediated Gut-Brain Axis in Post-Stroke Cognitive Impairment

WAN Chen lei, REN Binbin

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Post-stroke cognitive impairment (PSCI) is a common and debilitating complication following stroke,involving complex mechanisms such as neuroinflammation,neurotransmitter imbalance, and impaired neural plasticity. Recently,the vagus nerve (VN)-mediated gut-brain axis (GBA), a vital bidirectional communication pathway between the central nervous system and the gut, has gained increasing attention for its pivotal role in the onset and recovery of PSCI. The vagus nerve modulates gut microbiota homeostasis, intestinal barrier integrity, and immune responses, thereby indirectly affecting central nervous system inflammation and neural plasticity. Stroke can disrupt vagal signaling, resulting in gut microbiota dysbiosis and altered metabolite production, which further trigger central inflammatory responses and worsen cognitive dysfunction. This review synthesizes current evidence on the mechanisms of the VN-mediated gut-brain axis (VN-GBA) in PSCI and their interconnected relationships, and explores targeted intervention strategies that may offer promising therapeutic avenues for managing post-stroke cognitive impairment. These insights aim to contribute to the clinical prevention and treatment of PSCI.
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Research Progress on Biomaterials and Tissue Engineering in the Context of Treating Traumatic Brain Injury

WU jianfei, LIU yu, WANG binyou, XU maoya, WANG yilin, CAI duanfang, TAN youguo, LIU kezhi

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Traumatic Brain Injury (TBI) is a leading global cause of mortality and neurological dysfunction, characterized by a dynamic pathological process primarily involving primary injury and secondary injury. External mechanical forces directly inflict the primary injury, causing extensive vascular disruption and widespread shearing disruption of axonal fibers in white matter, which triggers cerebral hemorrhage and cellular damage; this is followed by secondary injury, where neuronal degeneration, chronic neuroinflammation, and mitochondrial dysfunction further exacerbate the pathology. Current clinical strategies such as surgical intervention, hyperbaric oxygen therapy, and dietary interventions offer only symptomatic treatment and fail to significantly improve long-term prognosis, necessitating innovative alternative therapeutic approaches and effective delivery strategies. The emergence of tissue engineering provides promising alternatives through the use of biomaterials including hydrogels, electrospun nanofibers, and nanoparticle based drug delivery systems. These biomaterials can construct biomimetic microenvironments, overcome blood brain barrier (BBB) delivery limitations, and enable multilevel synergistic modulation of neural repair. This review aims to synthesize recent advances in tissue engineering for TBI treatment, analyze therapeutic efficacy and underlying mechanisms, and provide novel insights for future research.
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Time-restricted feeding improves metabolic dysfunction-associated steatohepatitis by inhibiting ferroptosis through the Sirt1/Nrf2 pathway

LI Shengnan, FAN Dandan, SONG Weifang

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Objective To investigate the effects of time-restricted feeding (TRF) on improving metabolic-associated steatohepatitis (MASH) and its underlying molecular mechanisms. Methods (1) A MASH model was established in C57BL/6J mice using a high-fat, high-cholesterol diet. Twenty-four mice were randomly assigned to four groups: normal control (NC), normal time-restricted feeding (NT), model (M), and model time-restricted feeding (MT), with six mice per group. After 14 weeks of rearing, mice were anesthetized, weighed, and serum samples were collected. Serum levels of total cholesterol (TC), triglycerides (TG), aspartate aminotransferase (AST), alanine aminotransferase (ALT) , malondialdehyde (MDA), and ferrous ions (Fe2?) were measured. Livers were harvested and the liver index was calculated. Oil red O, hematoxylin-eosin (HE), and Masson's trichrome staining were used to evaluate the degree of hepatic steatosis, inflammatory infiltration, and fibrosis. Protein expression levels of SIRT1, Nrf2, ACSL4, TfR1, SLC7A11, glutathione peroxidase 4 (GPX4), and tumor necrosis factor alpha (TNF-α) were detected by western blot. (2) An in vitro MASH model was established in HepG2 cells using oleic acid and cholesterol stimulation, and a fasting model was established via serum deprivation. The experimental cells were divided into the control group, serum-deprived (FBS-) group, M group, and M+FBS- group. The ferrostatin-1 (Fer-1) ferroptosis inhibitor was employed to investigate the relationship between ferroptosis and MASH/TRF. Sirt1 activity was inhibited using the Sirt1 inhibitor compound EX-527 to investigate the relationship between Sirt1 and Nrf2-mediated ferroptosis. Lipid accumulation in hepatocytes was observed via Oil Red O staining. HepG2 cell levels of TC, TG, ALT, and AST were measured using kits. Western blot analysis assessed the protein expression levels of Sirt1, Nrf2, TfR1, ACSL4, SLC7A11, GPX4, and TNF-α expression levels in HepG2 cells. Results (1) Compared with MASH mice, TRF significantly reduced body weight and serum levels of TC, TG, ALT, AST, MDA, and Fe2? (P < 0.01). Liver Fe2? levels and TNF-α expression were also markedly decreased (P<0.01), while hepatic steatosis and fibrosis were improved. Western blot analysis revealed that TRF intervention significantly increased Sirt1, Nrf2, SLC7A11, and GPX4 protein levels(P < 0.01) while decreasing TfR1 and ACSL4 protein levels in the livers of MASH mice (P < 0.01). (2) Compared with the M group, serum deprivation intervention reduced TC, TG, ALT, AST, MDA levels, and TNF-α expression in oleic acid-cholesterol-induced HepG2 cells (P < 0.01), effectively reducing the number of lipid droplets. Western blot analysis indicated that serum deprivation intervention markedly elevated Sirt1, Nrf2, SLC7A11, and GPX4 protein levels(P < 0.01) while markedly decreasing TfR1 and ACSL4 protein levels (P < 0.01). Following Fer-1 intervention, SLC7A11 and GPX4 protein levels markedly increased(P < 0.01), while TfR1 and ACSL4 protein levels effectively reduced (P < 0.01). Following EX-527 intervention, Sirt1, Nrf2, SLC7A11, and GPX4 protein levels substantially decreased(P < 0.05 or P < 0.01), while TfR1 and ACSL4 protein levels significantly increased(P < 0.01), markedly attenuating the ameliorative effects of serum deprivation on fat accumulation and injury in the M group (P < 0.05 or P < 0.01). Conclusions TRF may improve metabolic-associated fatty liver disease by inhibiting ferroptosis, with its protective mechanism potentially involving the Sirt1/Nrf2 pathway it mediates.
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Study on the mechanism of the NRF2 pathway in the damage to spermatogonia caused by combined exposure to black carbon and palmitic acid

Zhang yuan, Han xue, Shi jinke, Wu desheng, Huang haiyan, Liu jianjun

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Objective To investigate the effects and modes of action of combined exposure to black carbon and palmitic acid on mouse spermatogonia GC-1, as well as the role of NRF2 pathway in the damage caused by this combined exposure. Methods A control group, palmitic acid groups(PA), black carbon groups(BC) and combined action groups were set up. Mouse spermatogonia GC-1 cells were treated with PA and BC for 24 h. The cell viability was assessed using by CCK-8 detection method. Real-time quantitative PCR (RT-qPCR) was used to detect the mRNA expression levels of nuclear factor erythroid 2-related factor (NRF2), Kelch-like ECH-related protein 1 (KEAP1), catalase (CAT), heme oxygenase-1 (Hmox1), quinone oxidoreductase 1 (NQO1), glutamyl cysteine ligase (GCLC), autophagy-related genes (Lc3b, P62), and ferroptosis-related genes glutathione peroxidase 4 (GPX4). The content of lipid oxidation (MDA) and reduced glutathione(GSH)were determined by colorimetric method. Results With the increase in exposure concentration, the inhibitory effect of PA and BC on the proliferation of GC-1 cells was enhanced, the IC50 values of PA and BC on GC-1 cells after 24 h were 320μmol/L and 560μg/mL, respectively. When PA was combined with BC, its IC50 for GC-1 cells was lower than that of the single-agent group, indicating a synergistic effect. The results of RT-qPCR showed that after 24 h of PA and BC exposure, both alone and in combination, the expressions of the antioxidant stress-related genes NRF2, KEAP1, CAT, Hmox1, NQO1, GCLC, ferroptosis-related genes GPX4, autophagy-related genes Lc3b and P62 were changed compared with the control group. The expression of NRF2 and Hmox1 was up-regulated (P<0.05), and KEAP1 was down-regulated(P<0.05). The expression of CAT was increased, except in the 20μmol/L PA group and the 40μmol/LPA group (P<0.05). The expression of NQO1 was increased, except in the 20μmol/L PA, 70μg/mL BC and 280μg/mL BC groups (P<0.05). The expression of GCLC was increased, except in the 20μmol/L PA group and the BC group (P<0.05). The expression of ferroptosis-related gene GPX4 was increased, except in the 20μmol/L PA group and the 40μmol/LPA group (P<0.05). The expression of autophagy-related genes Lc3b and P62 was increased, except in the 20μmol/L PA group and the 40μmol/LPA group (P<0.05). The content of MDA in each group was higher than that in the control group (P<0.01),while the content of GSH in each group was lower than that in the control group (P<0.01). Conclusions Both PA and BC can inhibit the proliferation of spermatogonia, and when the two are present simultaneously, they have a synergistic effect and enhance cytotoxicity. The combination of low-level PA and BC exposure to spermatogonia for 24 h triggered an early adaptive response, the mRNA expression level of antioxidant stress-related gene KEAP1 decreased, while the mRNA expression level of NRF2, Hmox1, NQO1, GCLC and CAT increased, the mRNA expression level of ferroptosis-related gene GPX4 increased, the mRNA expression level of autophagy-related genes P62 and Lc3b increased. The content of MDA in cells increased, and the content of GSH decreased. It causes the cells to react to oxidative stress and suggests that the NRF2 pathway may be involved in regulating the process of damage to spermatogonia caused by the combined exposure to PA and BC.
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Exploring the mechanism by which genistein alleviates alcoholic fatty liver disease based on the SIRT1/SIRT3 -FOXO1 signaling pathway

Zou Yingjie, Liu Jiangli, Yi Xu, Wu Xueli, Wang Shuoshi, You Shaowei

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Objective: To investigate the mechanism of genistein (GEN) in ameliorating alcoholic fatty liver disease (AFLD) through regulation of the Sirtuin1(SIRT1)/Sirtuin3(SIRT3)-Forkhead Box Protein O1(FOXO1) signaling pathway. Methods: An in vitro AFLD model was established by treating HepG2 cells with 100 μmol/L oleic acid combined with 150 mmol/L 95% ethanol. The experiment was divided into 16 groups, including: control group, model group, genistein group, resveratrol group, SIRT1 gene silencing control group (C-shSIRT1), SIRT3 gene silencing control group (C-shSIRT3), SIRT1 gene silencing model group (M-shSIRT1), SIRT3 gene silencing model group (M-shSIRT3), SIRT1 gene silencing genistein group (G-shSIRT1), SIRT3 gene silencing genistein group (G-shSIRT3), SIRT1 gene silencing resveratrol group (R-shSIRT1), SIRT3 gene silencing resveratrol group (R-shSIRT3), SIRT1/SIRT3 double gene silencing control group (C-shSIRT1/3), SIRT1/SIRT3 double gene silencing model group (M-shSIRT1/3), SIRT1/SIRT3 double gene silencing genistein group (G-shSIRT1/3), and SIRT1/SIRT3 double gene silencing resveratrol group (R-shSIRT1/3). The optimal intervention concentrations of genistein and resveratrol were screened by CCK-8 assay. Cellular steatosis was analyzed through Oil Red O staining and measurements of triglyceride (TG), total cholesterol (TC), and free fatty acid (FFA) levels. Intracellular levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) were determined by ELISA. Western blot was used to detect the protein expression levels of SIRT1, SIRT3, and FOXO1 in each experimental group, and the interactions among these three proteins were analyzed by co-immunoprecipitation (Co-IP) technique. Results: Genistein significantly ameliorated lipid deposition and inflammatory response in HepG2 AFLD model cells (P<0.05). Compared with the control group, the protein expressions of SIRT1, SIRT3 and FOXO1 were significantly decreased in the model group (P<0.01); while compared with the model group, the genistein group showed significantly increased protein expressions of SIRT1, SIRT3 and FOXO1 (P<0.05). The Co-IP results showed that SIRT1, SIRT3 and FoxO1 interacted with each other. Genistein significantly ameliorated cellular steatosis after either SIRT1 or SIRT3 gene silencing, but its anti-AFLD effect was markedly attenuated when both SIRT1 and SIRT3 genes were simultaneously silenced. Compared with the C-shSIRT1 group, FOXO1 expression level was significantly increased in the M-shSIRT1 group (P<0.01). Compared with the M-shSIRT1 group, FOXO1 expression was significantly decreased in the G-shSIRT1 group (P<0.01). Compared with the C-shSIRT3 group, FOXO1 expression was significantly decreased in the M-shSIRT3 group (P<0.0001). Compared with the M-shSIRT3 group, FOXO1 expression was significantly increased in the G-shSIRT3 group (P<0.0001). Compared with the C-shSIRT1/3 group, FOXO1 expression was significantly decreased in the M-shSIRT1/3 group (P<0.001); FOXO1 expression levels were similar between the M-shSIRT1/3 group and G-shSIRT1/3 group (P>0.05). Conclusions: Genistein ameliorates lipid metabolism and suppresses inflammatory response in HepG2 AFLD cells by regulating the SIRT1/SIRT3-FOXO1 signaling pathway, especially suggesting that regulating SIRT3-FOXO1 signaling plays a significant role in genistein anti-AFLD.
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Exploring the Effects of Xiongmatang Active Ingredients on Gut Microbiota in Migraine Rats Based on 16S rDNA

HE Qi, CHANG Lulu, LIUDingding, ZENG Guirong, CHEN Weishi, JIANG Ning, LIU Dong, WU Xuemei, WU Yuanhua

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【Abstract】Objective To study the effect of active ingredients of Xiongmatang on intestinal microbes in migraine rats. Methods 120 rats underwent dural cannulation surgery, observing the general physical signs of rats, 90 rats with better living conditions were selected and injected with inflammation soup 6 times within 12 days to stimulate the dura mater to replicate the migraine model, and were randomly divided into 9 groups: Model group, CGRP inhibitor group, Flunarizine positive group, the active ingredients of Xiongmatang(Low-dose group of n-butanol extract of Xiongmatang, High-dose group of n-butanol extract of Xiongmatang, Low-dose group of ethyl acetate extract of Xiongmatang, High-dose group of ethyl acetate extract of Xiongmatang, Low-dose group of n-butanol + ethyl acetate extract of Xiongmatang, High-dose group of n-butanol + ethyl acetate extract of Xiongmatang), 10 each group. Another 10 rats were injected with 0.9% sodium chloride solution in the same way as Control. After successful modeling, the blank group and the model group were given Pure water by gavage, and the rats in the CGRP inhibitor group were given administration by tail vein, once a week, for a total of 5 times; the other groups were given corresponding drugs, once a day, for a total of 4 weeks (28 d). At the end of the drug administration period, behavioral assessments were conducted using sucrose preference test, tail suspension test, novel object recognition test, and Morris water-maze test. Abdominal aortic blood was collected for ELISA quantification of circulating CGRP and NO levels. Intestinal contents were taken, and the changes in the gut microbiota of rats were analyzed by 16S rDNA high-throughput sequencing technology. Results Compared with the control group, model group rats exhibited significant depressive-like behavioral changes and cognitive impairments. Meanwhile, the contents of CGRP and NO in serum were significantly increased . Gut microbiota analysis revealed marked alterations in microbial community structure, at the phylum level, the community abundance of Firmicutes, Actinobacteriota, Unclassified and Campylobacterota decreased significantly. The community abundance of Bacteroidota, Verrucomicrobiota, Patescibacteria and Cyanobacteria increased significantly . At the genus level, community abundances such as Muribaculaceae_unclassified and Lactobacillus were significantly decreased . The community abundances of Ruminococcus, Clostridia_UCG-014_unclassified, Akkermansia, Firmicutes_unclassified and Monoglobus were significantly increased. Compared with the model group, the CGRP inhibitor group, flunarizine positive group, the active ingredients of Xiongmatang dose-dependently reversed the depressive-like behavioral changes and cognitive impairments observed in migraine rats, and significantly lowered serum levels of CGRP and NO. The active ingredients of Xiongmatang treatment also modulated intestinal microbial diversity: α-diversity assays showed increased richness and evenness, asβ-diversity revealed that the microbial community structure of XMT-treated rats closely resembled that of the blank group. At both phylum and genus levels, the alterations in microbiota composition exhibited trends opposite to those seen in the model group. Conclusions The active ingredients of Xiongmatang may prevent and treat migraine in rats by regulating the gut microbiota.
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Establishment of an Indirect ELISA for Serological Diagnosis of Lyme Disease in Mice

ZHAI Bintao, BAO Bibo, MA Shaoxia, LI Jia, ZHOU Yaxin, LI Bing, ZHANG Jiyu

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This study established an indirect ELISA-based serological diagnostic method for Lyme disease in mice, using whole-cell antigens of Borrelia garinii strain SZ. Through systematic optimization of experimental conditions, the optimal reaction system was determined as follows: antigen coating concentration of 0.2 μg/μl, serum dilution ratio of 1:200, and enzyme-labeled secondary antibody concentration of 1:2000. This method ensured high sensitivity (OD value > 0.8) while significantly reducing antigen consumption. Antibody dynamic analysis revealed that serum antibody levels in infected mice peaked between 12–25 days post-inoculation, with a specificity antibody ratio (ArB%) threshold of 41.7% to distinguish positive and negative samples. The study also evaluated cross-reactivity between B. garinii and Borrelia burgdorferi (B31) strain as well as Borrelia afzelii (BO23)strain, indicating certain cross-reactivity with BO23 but no significant cross-reactivity with B31. The results demonstrated that this method is simple, cost-effective, and suitable for primary laboratories and small-scale screening. It provides a reliable standardized technical support for the laboratory diagnosis and epidemiological surveillance of Lyme disease.
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Experimental Study on the Inhibition of Colon Tumor Growth by Autologous Microbiota Transplantation and Its Regulation of Tight Junction Proteins

renhang, baijing, zhangjunqi, yexueshuai, tanmengtian, sunyuhang, lilei, fuzexian

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To observe the colonic tumor status in mice with azoxymethane/dextran sodium sulfate (AOM/DSS)-induced colitis-associated colorectal cancer (CAC) following autologous fecal microbiota transplantation (AFMT) intervention, and to investigate the anti-tumor effects and underlying mechanism of AFMT through its influence on tight junction proteins. Methods: Female BALB/c mice (SPF grade) were randomly divided into three groups (n=8 each): the Blank Control group, the CAC Model group, and the AFMT Intervention group. The CAC Model group received a single intraperitoneal injection of AOM (10 mg/kg), followed by drinking water containing 3.5% DSS for 7 days, and then 0% DSS for 14 days, constituting one cycle; three cycles were performed to establish the CAC model. The AFMT Intervention group received daily AFMT (0.1 mL autologous fecal suspension) via gavage every other day concurrent with the CAC modeling protocol until cycle completion. The Blank Control group received no special treatment. The general condition and body weight of the mice were monitored. Upon completion of the experiment, colon length was measured and tumor numbers were recorded. Colon pathological examinations were performed. The mRNA and protein expression levels of tight junction proteins Occludin (Ocln) and Claudin-1 (Cldn1) in colorectal tumor tissue were detected using RT-qPCR and Western blotting, respectively. Fecal microbiota composition from each group was analyzed using 16S rRNA gene sequencing. Results: Compared to the Blank Control group, the CAC Model group exhibited significantly shortened colon length and a significant increase in tumor number. After AFMT intervention, the shortening of colon length was alleviated and the tumor number decreased significantly compared to the CAC Model group. Histological examination revealed distorted crypt architecture, reduced goblet cells, and increased inflammatory cell infiltration in the colons of the CAC Model group. Following AFMT intervention, crypt architecture and goblet cell numbers showed improvement, with decreased inflammatory cells. Compared to the Blank Control group, the mRNA and protein expression levels of Ocln (Occludin) and Cldn1 (Claudin-1) were significantly reduced in colorectal tumor tissue of the CAC Model group. AFMT intervention significantly increased the mRNA and protein expression levels of Ocln (Occludin) and Cldn1 (Claudin-1) compared to the CAC Model group. Fecal microbiota analysis showed no statistically significant difference in Firmicutes abundance between the AFMT Intervention group and the Blank Control group, while the CAC Model group had a significantly lower Firmicutes abundance compared to the Blank Control group. No statistically significant difference in Bacteroroidota abundance was found between the AFMT Intervention group and the Blank Control group, but the CAC Model group exhibited significantly higher Bacteroroidota abundance than the Blank Control group. Conclusion: AFMT intervention can restore Firmicutes abundance and reduce Bacteroroidota abundance in the gut, effectively improve the aberrant expression of tight junction proteins within the tumor microenvironment, repair the intestinal barrier, regulate the intestinal functional barrier, alleviate intestinal inflammation, and consequently mitigate the pathological progression of CAC.
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A Comparative Study on the Stability of DOCA-Salt Hypertensive Rat Experimental Animal Models

wangweiwei, liuxiaoran, lifengxin, wuyi, sunzhenguo

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Aim: This study aimed to evaluate the feasibility of establishing a hypertensive rat model induced by deoxycorticosterone acetate (DOCA), and to compare the model stability between a surgical group (unilateral nephrectomy combined with DOCA injection) and a non-surgical group (DOCA injection alone). Method: Healthy Wistar rats were randomly divided into a surgical group and a non-surgical group according to body weight. Rats in the surgical group underwent left nephrectomy followed by subcutaneous injection of DOCA (50 mg/kg), five times per week for five weeks. Rats in the non-surgical group received DOCA injections following the same protocol for seven weeks without nephrectomy. Both groups were given free access to 1% saline solution throughout the experiment. Tail artery blood pressure was monitored weekly until week 10. Blood pressure changes and model stability were compared between the groups. Results: Results showed that systolic blood pressure reached the hypertensive threshold by week 5 in the surgical group and by week 7 in the non-surgical group. By week 10, both groups maintained elevated blood pressure levels, indicating good model stability. Conclusion: These findings suggest that subcutaneous DOCA administration can effectively induce hypertension in rats without the need for nephrectomy. Compared with the conventional surgical model, the non-surgical method is simpler, safer, reproducible, and has broad applicability for hypertension research.
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Exploring the improvement mechanism of Sijunzi Tang on osteosarcopenia rats based on TLR4/NF-κB pathway

Ou Fan

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Objective: To explore the improvement mechanism of Sijunzi Tang on osteosarcopenia (OS) rats based on TLR4/NF-κB pathway. Methods: Rats were assigned into sham operation group, OS group, low-dose Sijunzi Tang group, high-dose Sijunzi Tang group, estradiol group and high-dose Sijunzi Tang+lipopolysaccharide (LPS) group randomly. The OS model was constructed by castration combined with intraperitoneal injection of dexamethasone. After treatment with Sijunzi Tang and TLR4 activator LPS, the forelimb muscle strength, whole-body and femoral bone densities, muscle percentage, and distal femoral bone microstructure [percent bone volume (BV/TV), bone surface density (BS/TV), trabecular number (Tb.N), and trabecular separation degree (Tb.Sp)] were measured. The mass fraction of quadriceps muscle was detected, and HE staining was used for histopathological examination of quadriceps muscle tissue. The cross-sectional area (CSA) of quadriceps muscle fibers was compared. ELISA was used to measure serum procollagen i n-terminal propeptide (PINP), C-telopeptide of type I collagen (CTX-1), osteocalcin (OCN) ?and inflammatory factors. Immunohistochemical staining and immunoblotting was used to detect TLR4/NF-κB pathway proteins in the quadriceps femoris and femoral tissues. Results: For the sham surgery group, the OS group showed a decrease in forelimb muscle strength, whole-body and femoral bone densities, muscle percentage, BV/TV, BS/TV, Tb.N, quadriceps mass fraction and muscle fiber CSA, the levels of PINP and OCN (P<0.05), and an increase in Tb.SP, the levels of CTX-1, IL-6, IL-1β and IL-17, positive expression of TLR4 and p-NF-κB p65, TLR4 protein expression, p-NF-κB p65/NF-κB p65 (P<0.05). For the OS group, the low and high-dose Sijunzi Tang groups, estradiol group showed an increase in forelimb muscle strength, whole-body and femoral bone densities, muscle percentage, BV/TV, BS/TV, Tb.N, quadriceps mass fraction and muscle fiber CSA, the levels of PINP and OCN (P<0.05), and a decrease in Tb.SP, the levels of CTX-1, IL-6, IL-1β and IL-17, positive expression of TLR4 and p-NF-κB p65, TLR4 protein expression, p-NF-κB p65/NF-κB p65 (P<0.05). However, high-dose Sijunzi Tang and estradiol had a stronger improvement effect on various pathological indicators in OS rats. For the high-dose Sijunzi Tang group, the high-dose Sijunzi Tang+LPS group showed a decrease in forelimb muscle strength, whole-body and femoral bone densities, muscle percentage, BV/TV, BS/TV, Tb.N, quadriceps mass fraction and muscle fiber CSA, the levels of PINP and OCN (P<0.05), and an increase in Tb.SP, the levels of CTX-1, IL-6, IL-1β and IL-17, positive expression of TLR4 and p-NF-κB p65, TLR4 protein expression, p-NF-κB p65/NF-κB p65 (P<0.05). There was no significant change in various indicators between the high-dose Sijunzi Tang group and the estradiol group (P>0.05). Conclusion: Sijunzi Tang can improve muscle atrophy and osteoporosis symptoms in OS rats by suppressing activation of TLR4/NF-κB signaling pathway.
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Possible mechanisms underlying improvement of autism-like behaviors by melanotan-II in Shank3-deficient rats

Chen Xiaofang, Wang Juan, Chen Sijie, Ou Ping, Huang Longsheng

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Objective:?To explore the mechanism by which Melanotan-II (MT-II) improves social deficits in a Shank3 gene-deficient autism model. Methods:?A Shank3-deficient rat model (n=20) and a control group (n=20) were established by microinjecting Shank3-interfering lentivirus or empty lentivirus, respectively, into the right lateral ventricle of neonatal rats. The Shank3-deficient rats were randomly divided into two groups: the Shank3+Saline (Sh3-Sal) group (n=9) and the Shank3+MT-II (Sh3-MT-II) group (n=9). Similarly, the control rats were divided into the Control+Saline (V-Sal) group (n=9) and the Control+MT-II (V-MT-II) group (n=9). On day 28, the V-MT-II and Sh3-MT-II groups received intraperitoneal (i.p.) injections of MT-II (3.3 mg/kg), while the V-Sal and Sh3-Sal groups received i.p. saline (3.3 ml/kg). Behavioral changes were assessed using the open field test, grooming behavior analysis, the three-chamber social test, and the Morris water maze test. The mRNA and protein expression levels of hypothalamic oxytocin (OXT), oxytocin receptor (OXTR), and melanocortin receptor 4 (MC4R) were detected by reverse transcription polymerase chain reaction (RT-PCR) and Western blot, respectively. Results:?In the three-chamber social test, compared to the time spent with stranger rat 1, the Sh3-Sal group showed no significant social preference (P > 0.05). In contrast, after MT-II intervention, the Sh3-MT-II group spent significantly more time with stranger rat 2 (P < 0.01). In the Morris water maze test, the Sh3-Sal group exhibited significant learning and memory impairments compared to the V-Sal group (P < 0.05). MT-II intervention significantly improved the learning and memory performance of the Sh3-MT-II group (P < 0.01). The open field and grooming tests revealed that compared to the V-Sal group, the Sh3-Sal group spent significantly more time in the peripheral zone of the open field and exhibited increased grooming behavior (P < 0.01). However, MT-II intervention did not significantly alter the center time or self-grooming behavior compared to the Sh3-Sal group (P > 0.05). RT-PCR analysis showed that the mRNA expression levels of OXT, OXTR, and MC4R in the Sh3-MT-II group were significantly higher than those in the Sh3-Sal group (P < 0.05). Western blot analysis indicated that hypothalamic OXT protein expression was significantly increased in the Sh3-MT-II group compared to the Sh3-Sal group (P < 0.05). Compared to the V-Sal group, hypothalamic SHANK3 protein expression was significantly decreased in both the Sh3-Sal and Sh3-MT-II groups (P < 0.05), while the protein expression levels of OXTR and MC4R showed no significant changes (P > 0.05). Conclusion:?The melanocortin receptor agonist MT-II may ameliorate social deficits in Shank3-deficient autistic rats by activating the hypothalamic OXT system. This finding suggests that targeting the OXT/MC4R pathway could be a potential therapeutic strategy for social deficits in autism spectrum disorder.
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ACSL4-mediated ferroptosis is involved in early aging-related cardiac hypertrophy and fibrosis

Feng Tao, Chen Hong, Deng Yuxiao, Zhou Zhiyi, Fang Xiaoyan, Li Biao, Wang Jinhua, Liao Suchan

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Objective This study aims to preliminarily explore the role of mitochondria-related programmed cell death mechanisms, including apoptosis, autophagy, and ferroptosis, in early aging cardiac hypertrophy and myocardial fibrosis. Methods Male young C57BL/6 mice (5 months old, n=6) and early aging mice (21 months old, n=6) were housed in a specific pathogen-free (SPF) environment. Cardiac tissues were collected for micro-CT scanning imaging. Paraffin sections were subjected to H E and Van Gieson staining. Cardiac mitochondria were extracted to measure reactive oxygen species (ROS) levels and the expression of dynamics-related proteins dynamin-related protein 1 (Drp1), mitofusin 2 (Mfn2), and optic Atrophy 1 (OPA1). The ultrastructure of mitochondria was observed using transmission electron microscopy. Western blot analysis was performed to assess the protein expression levels of inflammatory markers receptor-interacting serine/threonine-protein kinase 3 (RIP3) and phosphorylated Nuclear Factor kappa B (p-NF-κB), fibrosis marker collagen type I (Collagen I), apoptosis markers cysteinyl aspartatespecific protease-3 (Caspase-3) and cleaved cysteinyl aspartatespecific protease-3 (Cleaved caspase-3), autophagy markers phosphorylated protein kinase B (p-Akt), protein kinase B (Akt), and microtubule-associated protein 1 light chain 3 I/II (LC3I/II), as well as ferroptosis markers acyl-coa synthetase long-chain family member 4 (ACSL4) and solute carrier family 7 member 11 (SLC7A11). Results Compared with young mice, early-aged mice exhibited myocardial hypertrophy and fibrosis, disordered cardiomyocyte arrangement, increased mitochondrial ROS levels, and no significant changes in the expression of the mitochondrial fission-related protein Drp1. However, there was an increased expression of the fusion-related proteins Mfn2 and OPA1. Electron microscopy revealed that myocardial mitochondria displayed swelling and disordered cristae structures. The expression of the myocardial fibrosis marker Collagen I was found to be elevated, alongside an increase in the inflammation-related markers RIP3 and p-NF-κB. In contrast, the expression of the autophagy-related protein LC3 II was reduced, while no significant change was observed in the expression of the apoptosis-related protein cleaved caspase-3. Additionally, the expression of the ferroptosis-related protein ACSL4 was increased, whereas the expression of SLC7A11 was decreased. Conclusion Early cardiac aging is characterized by hypertrophy and myocardial fibrosis, which are accompanied by inflammation, mitochondrial dysfunction, and kinetic imbalance. Notably, ferroptosis, rather than apoptosis, emerges as the primary pathway of programmed cell death during the early stages of cardiac aging.
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RAD23B promotes colorectal cancer metastasis via the Talin1/Integrin/PI3K/AKT/MMP9 axis

chenyang, lijuan, haozhijiao, xiehairu, zhengyutong, wuchenpeng, fanjingyi, lijun

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Objective RAD23B, a DNA repair-related protein, has been implicated in the progression of various malignancies. This study aimed to investigate the role of RAD23B in promoting colorectal cancer (CRC) metastasis and to elucidate the underlying molecular mechanisms.Methods RAD23B was overexpressed in CRC cell lines SW480 and HCT-8, with empty vectors serving as controls.Cell proliferation, migration, and invasion were assessed using Cell Counting Kit-8 (CCK-8) and Transwell assays.A xenograft mouse model was used to evaluate metastatic potential in vivo.Transcriptomic analysis by RNA sequencing (RNA-seq) was performed to identify signaling pathways regulated by RAD23B.Western blotting was used to analyze the expression of RAD23B, Talin1, Integrins αv/β1, phosphoinositide 3-kinase (PI3K), phosphorylated PI3K (p-PI3K), protein kinase B (AKT), phosphorylated AKT (p-AKT), and matrix metalloproteinase 9 (MMP9).Results RAD23B overexpression significantly enhanced CRC cell proliferation, migration, and invasion both in vitro and in vivo.RNA-seq revealed that RAD23B upregulated Talin1 and Integrins αv/β1, leading to activation of the PI3K/AKT signaling pathway. Moreover, RAD23B promoted MMP9 expression, contributing to enhanced invasive potential.Conclusion RAD23B promotes colorectal cancer liver metastasis through activation of the Talin1/Integrin/PI3K/AKT/MMP9 axis.
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The Impact of Hypoxia-Reoxygenation on Endoplasmic Reticulum Stress in Hippocampal cell line*

guan lu, ge rili, Mashuang

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To investigate the effects of hypoxia-reoxygenation (H/R) on hippocampal neurons and endoplasmic reticulum stress in mice. HT22 hippocampal neurons were used for subsequent experiments after H/R treatment. CCK8 and scratch test were used to detect the proliferation and migration of HT22 hippocampal neurons to observe the effect of H/R on HT22 hippocampal neurons. The effect of H/R on the morphology of endoplasmic reticulum was observed by transmission electron microscopy, and the effect of H/R on the development of HT22 hippocampal neurons was observed by immunofluorescence. Western-Blot and qRT-PCR were used to observe the effect of H/R on endoplasmic reticulum stress in hippocampal neurons. The results showed that compared with the control group, H/R inhibited the proliferation and migration of HT22 hippocampal neurons, and the expression of neurodevelopmental protein BDNF was decreased. In addition, H/R also reduced the expression of synaptic plasticity proteins PSD-95 and α-Syn. The effect of H/R on ER stress is reflected in the swelling of ER caused by H/R, which promotes the expression of ER stress signals such as GRP94, BIP and ATF6. Therefore, H/R has a damaging effect on HT22 hippocampal neurons, which may be related to enhanced ER stress.
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Construction and optimization of an in vitro model based on tissue-specific hypoxic injury exploration

maziru, yuxueqing, yanruonan, tanghuimeng, huhaiyang, zhaowenhan, yangshuguang

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Hypoxia is an important part of the pathogenesis of many chronic respiratory diseases, cardiovascular diseases, cerebral ischemia and solid tumors and other major diseases. Cell hypoxia mode is an important tool to analyze the mechanism of hypoxia response and screen potential therapeutic targets. The scientificity and applicability of its construction directly affect the reliability of the research conclusions, and are of great significance to the development of related disease prevention and treatment research. At present, the research on the construction and application of cell hypoxia model has achieved stage-by-stage results, but there are still some limitations in the model evaluation system and tissue cell specificity. This paper summarizes the current status of research on the mechanism of hypoxia occurrence and development and evaluation of indicators, combines the tissue-specific characteristics, and discusses the construction and optimization of the cellular hypoxia model, which provides a reference for the construction of the model, and assists in the research and development and translation of targeted therapies.
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Research on the Construction of Ideological and Political Education System for 'Pathogenic Biology' Courses under the Concept of ' One_Health '

liujixin, Sunyanhong, Zhaoyuanyuan, Lvliyan, Zhanghao

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【】The "Healthy China 2030" plan clearly states that "jointly building and sharing, and promoting health for all" is the strategic theme of building a healthy China. It is necessary to promote extensive participation from the whole society, strengthen cross-departmental collaboration, enhance environmental governance, ensure food and drug safety, prevent and reduce harm, and effectively control ecological and social environmental risk factors that affect health. Medical education is a crucial support for the health sector and a core component of the Healthy China strategy. Therefore, medical institutions must focus on deepening comprehensive reforms around the Healthy China strategy, adopt a broad perspective on education, health, and wellness. In recent years, especially following outbreaks like SARS, the "One_Health" education concept has emphasized from new perspectives, heights, and dimensions that human beings need to coexist harmoniously with other living beings and the environment to achieve true "health". As the main channel for disseminating the "One_Health" education concept in the new era, colleges and universities need to start from ideology, fully implement " One_Health " education, promote the construction of values, and give full play to the ideological and political education function of professional courses. The foundational medical course "Pathogenic Biology" serves as a bridge connecting core professional courses and is typically offered during a critical period of students" ideological education. This course has rich content, a broad audience, covers multiple knowledge areas, and offers numerous elements for integrating ideological and political education. How to incorporate the " One_Health" education concept into the ideological and political education system of the "Pathogenic Biology" course is the focus of this study.
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Crosstalk Between Metabolic Reprogramming and Inflammatory Coagulation: Novel Targets for Intervening in Deep Vein Thrombosis

LIU Cheng, ZHOU Tao

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Deep vein thrombosis (DVT) is the third most common cardiovascular disease in the world.Traditional anticoagulation therapy is limited. The pathophysiology of DVT usually focuses on Virchow triad, but it cannot explain many clinical problems, and the interaction between metabolic reprogramming and inflammation and coagulation may open up new perspectives for its theory. To explore the role of metabolic microenvironment in thrombosis and oxidative stress in metabolic reprogramming and thrombosis, analyze the feedback loop between metabolic reprogramming and inflammatory coagulation, summarize the therapeutic strategies of metabolic regulation intervention in DVT, including glucose metabolism, lipid metabolism intervention and antioxidant therapy, and point out the challenges faced by the therapeutic strategy level, providing a new way for the prevention and treatment of DVT.
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Application Progress in Performance Evaluation Models for HBOC in Circulation

ZHANG Yu, SU Chunyuan, WU Changtao, YANG Kang, ZHAO Huimin

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With the continuous deepening of global research and development of hemoglobin oxygen carriers (HBOCs), how to evaluate properly those performance in circulation is increasingly receiving attention. This article reviews the preparation methods, observation indicators, and performance evaluation of four main HBOC circulatory performance evaluation models, including shock model, isovolumetric blood replacement model, reperfusion injury model, and overload model, additionally provided suggestions on how to choose an appropriate model.
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The fluctuation of sex hormone levels during the female menopause stage promotes the development of Alzheimer""s disease

Ma TingXuan, YANG Huiling, XU Xiangyue, ZHANG Haiyan, JIANG Jiaxue, LIU Qing, LEI xia, XU Hongdan

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The levels of sex hormones in women during menopause are closely related to the progression of Alzheimer"s disease. The elevated levels of follicle-stimulating hormone and the decreased levels of estrogen jointly drive the pathological process of Alzheimer"s disease, including amyloid-β protein deposition, microtubule fibrillary tangles, neuroinflammation, and excessive activation of glial cells. This article elaborates on the relevant pathways and mechanisms by which the increase in FSH levels and the deficiency of estrogen during menopause exacerbate the pathological process of Alzheimer"s disease, providing a reference for the subsequent treatment of this disease.
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Research Advances in the Mechanism of Cellular Interactions in Ferroptosis-Mediated Idiopathic Pulmonary Fibrosis

LI Xinyi, FANG Liming, WANG Renzhe, WU Xiaolan, HU Weihua

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:Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease characterized by progressive scarring of the lung tissue, with a poor prognosis and a median survival of only 3–5 years.The precise molecular mechanisms underlying IPF remain incompletely elucidated, and effective targeted drugs are lacking. Therefore, defining its pathogenesis is crucial. Ferroptosis, a regulated form of cell death driven by iron-dependent lipid peroxidation, has been identified as a key player in IPF. Emerging studies into ferroptosis have revealed the roles of cell-cell interactions in IPF disease mechanisms at the cellular level. This article provides a summarized overview of the mechanism by which cellular interactions contribute to iron-dependent pulmonary fibrosis through ferroptosis.
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Acupuncture modulates programmed cell death in the treatment of Parkinson's disease

wangbinhan, Wuminmin, Liu Jiayu, Zhu Luwen

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Parkinson's disease is a common neurodegenerative disease characterized by progressive degeneration of nigrostriatal dopaminergic neurons and Lewy body morphology, the pathogenic mechanism is not yet fully understood, and with the rise in the number of patients, it places a huge burden on patients and society.. Acupuncture, a distinctive therapy in traditional Chinese medicine, has been widely used in the treatment of PD patients to improve motor and non-motor symptoms, and its mechanism may be closely related to the regulation of Programmed cell death-related signaling pathways. This article reviews the role of PCD in PD. PCD including apoptosis, necrotic apoptosis, cellular pyroptosis, iron death, and other forms, plays a key role in the process of neuronal damage in PD. Combined with the research progress of acupuncture intervention for PCD, it provides new ideas for clarifying the scientific connotation of acupuncture treatment for PD and developing new treatment strategies.
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Advances in the role of Mycobacterium tuberculosis in regulating macrophage death

matao, wulixian

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Macrophages, as intrinsic immune cells, are an important component of innate immunity and play an important role in immunity against Mycobacterium tuberculosis (Mtb) infection.After infecting the organism, Mtb mainly parasitizes macrophages, where it can survive and multiply, and induce different modes of cell death, including apoptosis, autophagy, pyroptosis, iron death, and necrotic apoptosis.Different modes of cell death play different roles in the process of Mtb infection. This paper provides a review of the different ways of macrophage death pathways and their roles after Mtb infection, with the aim of deepening the understanding of the potential impacts on host immunity during Mtb infection, and providing references for further research on the pathogenic mechanism of Mtb and the strategy of anti-tuberculosis treatment.
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A Preliminary Study on the Selection of CD19 and CD79A as Factors for Lung Adenocarcinoma Microenvironment Remodelling and Prognosis Using the Programmed Cell Death Genome in Combination with the TCGA Database

yujiaheng, chuyunqi, hongchaojin, linxingzi, xushengxia, liuyuehuan

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【Abstract】 Objective Lung adenocarcinoma (LUAD) has a poor prognosis. This study aimed to screen for core prognostic genes associated with the tumour microenvironment (TME) and programmed cell death (PCD) to provide new prognostic markers and therapeutic targets for LUAD and to validate their cross-species conservation. Methods Based on RNA-seq data from LUAD and normal lung tissue in the TCGA database, the ESTIMATE algorithm was used to assess the TME and screen for differentially expressed genes (DEGs). Functional enrichment (GO/KEGG) and protein-protein interaction (PPI) network analyses were performed on the DEGs. Core prognostic genes were identified through a combination of univariate COX regression and PCD genomic cross-screening. Their prognostic value and TME association were validated through survival analysis, genomic enrichment (GSEA), and immune infiltration (CIBERSORT) analysis. Results High immune/ESTIMATE scores were significantly associated with prolonged patient survival. The selected shared DEGs were primarily enriched in immune-related pathways. Cross-analysis identified CD19 and CD79A as core prognostic genes. Clinical feature analysis showed that CD19 and CD79A expression was significantly higher in LUAD tumour tissues than in normal lung tissues, but their expression levels decreased significantly with advancing TNM staging, closely associated with advanced staging, distant metastasis, and poor prognosis. Survival analysis indicated that LUAD patients with high CD19/CD79A expression had significantly longer overall survival than those with low expression. Animal experiment validation confirmed the cross-species conserved role of CD19/CD79A in tumour progression. GSEA analysis indicated that the high-expression group of CD19/CD79A was significantly enriched in immune activation pathways (such as allograft rejection and complement response), while the low-expression group was enriched in metabolic (glycolysis, oxidative phosphorylation) and oncogenic pathways. Immune infiltration (CIBERSORT) analysis further confirmed that their expression levels were significantly positively correlated with TME immune activity. Conclusion CD19 and CD79A are overexpressed in LUAD tumour tissues, but their expression levels decrease with disease progression. High expression of CD19/CD79A is closely associated with favourable prognosis and immune-activated TME, while low expression suggests poor prognosis and is associated with immune suppression/oncogenic states. They may serve as potential protective prognostic biomarkers and immunotherapy targets for LUAD, providing insights into LUAD immune mechanisms and guiding the development of B-cell-targeted therapeutic strategies.
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Exploring the Mechanism of LiqiTongfu Massage Massage Therapy on Functional Dyspepsia Rats Based on 4D-FastDIA Proteomics

Zhang Lidan, Shang Kun, Yang Zonghao, Cui Yidan, Yan Wenjian, Zhang Xin

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Objective:The 4D-FastDIA proteomic method was employed to explore how Liqitongfu massage works in treating functional dyspepsia (FD), focusing on the differences in proteins.Methods:30rats were categorized into three groups: blank, model, and massage, with each group containing 10 rats, determined by a random number table approach. Treatment for both the model and massage groups included tail clips, ice water, and a non-standard diet. After successful modeling, the massage group was treated with qi-tongfu manipulation. Following a 14-day treatment period, an assessment was conducted on the overall health and digestive movement of rats in every group, along with monitoring the pathological alterations in the rats" stomach tissues and identifying the protein levels in each.Results:General conditions: The blank group had good mental state and was active, while the model group had poor mental state, poor activity, and decreased gastric empelling rate and small intestinal propulsion rate. The massage group had improved mental state, activity rate, gastric empelling rate and small intestinal propulsion rate. HE staining results: No clear infiltration of inflammatory cells was observed in the gastric mucosa, nor was there a notable variance in gastric histopathology across the three groups. Results of the proteomic analysis: In contrast to the standard group, the model group exhibited alterations in 263 proteins, while the massage group showed changes in 237 proteins when compared to the model group. There were differences between the model group and the normal group, but the massage could reverse the difference trend of 95 proteins, of which 16 were up-regulated and 79 were down-regulated.Conclusion:Qitongfu massage can effectively improve FD, which may be related to the regulation of related target proteins.
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Exploring the Effects of Circadian Rhythm on Core Circadian Clock Genes in Insomnia Model Mice Based on Ying-Wei Theory

YANG Jing, HE Zong-qing, LIU Chi-xiao, ZHENG Yuxin, WANG Xiaoyan, LIU Feixiang, ZHAO Min

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Objective: To explore the regulatory effects of circadian rhythm disruption on circadian clock genes in the hypothalamus and amygdala at different time points in insomnia model mice based on Ying-Wei theory. Methods: 104 8-week-old female ICR mice were randomly divided into a normal group (n=52) and a model group (n=52), each further subdivided into subgroups at 6:00, 12:00, 18:00, and 24:00 (13 mice per time point). The model group received intraperitoneal injections of PCPA for 3 days, while the normal group received equivalent volumes of saline. Behavioral tests were conducted to evaluate sleep latency, total sleep duration, and anxiety-depression-like behaviors. Immunofluorescence staining was used to observe nuclear translocation of Period Circadian Regulator 1 (PER1) and Cryptochrome Circadian Regulator 1 (CRY1) in the hypothalamus and amygdala. RT-qPCR and Western blot were performed to measure mRNA and protein expression levels of circadian clock genes. Results: Compared with the normal group, the model group exhibited prolonged sleep latency, reduced sleep duration (P<0.01), decreased sucrose preference (P<0.01), increased grooming frequency, and extended central exploration distance in the open field test (P<0.01). Significant differences in mRNA and protein expression of core clock genes (PER1, CRY1, CLOCK, and BMAL1) were observed between the two groups at all time points, with inconsistent expression patterns between the hypothalamus and amygdala. In the model group, the peak nuclear co-localization of PER1 and CRY1 in the hypothalamus was advanced by 4–6 hours, while their nuclear co-localization peaks in the amygdala were phase-shifted by approximately 12 hours compared to the normal group. Conclusion: Dysregulated expression of core circadian clock genes in insomnia mice is associated with Ying-Wei imbalance-induced circadian rhythm disruption. The mechanism may involve differential nuclear dimerization of PER1 and CRY1 across brain regions.
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Expression of DLGAP5 in hypoxic pulmonary hypertension and its potential clinical value

LI Chen, LI Yi, WANG Xin, YUE Tianyuan, LUO Hanshen, JIANG Dingsheng, FANG Zemin

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Objective To explore the expression of disc large homology-associated protein 5 (DLGAP5) in the hypoxic pulmonary hypertension(HPH). Methods This study first used bioinformatics analysis to explore the expression of DLGAP5 in normal control group and HPH group. Then, lung tissue samples from 9 patients undergoing lung transplantation with HPH and 4 controls were collected, and the expression level of DLGAP5 in different lung tissues was detected by Western blot (WB). Rat models of Sugen5416 combined with chronic hypoxia(SuHx) was constructed to detect the mean pulmonary artery pressure(mPAP). The pulmonary vascular remodeling and the expression of DLGAP5 in HPH were detected by hematoxylin-eosin (HE) staining, immunohistochemistry (IHC) staining and immunofluorescence (IF) staining. Finally, differential gene enrichment analysis was used to explore the downstream signaling pathway of DLGAP5 regulating HPH. Results DLGAP5 was significantly upregulated in the lung tissue of HPH patients (P<0.05). The mPAP of SuHx-induced HPH model rats was significantly increased (P<0.05). The results of HE staining and IHC staining showed that the pulmonary artery media was thickened and obvious vascular remodeling occurred in the HPH model rats. The results of IF staining showed that compared with the control group, the expression of DLGAP5 in pulmonary artery media smooth muscle in HPH rats was increased (P<0.05), and it was mainly distributed in the cytoplasm. Finally, differential gene enrichment analysis, including GO and GSEA analysis, suggested that DLGAP5 may regulate HPH by influencing the cell cycle, especially the G2/M phase (P<0.05). Conclusions DLGAP5 may be a potential new target for HPH, bringing new ideas for the diagnosis and treatment of pulmonary hypertension.
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The Research Progress of the cGAS-STING Signaling Pathway in Inflammatory Pulmonary Diseases

Yang zihan, Yin Leyi, wangjunyang, maowei

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【】　The cGAS-STING signaling pathway is a crucial DNA recognition and signaling mechanism in the innate immune system, which is widely involved in the occurrence and development of immune-related diseases. However, in inflammatory lung diseases, excessive activation of this pathway may lead to chronic inflammation and tissue damage, thereby exacerbating or promoting disease progression. Currently, there is a lack of systematic research on the role of the cGAS-STING signaling pathway in these diseases. This review summarizes recent literature and systematically discusses the role of the cGAS-STING signaling pathway in inflammatory pulmonary diseases such as COPD, asthma, and pulmonary fibrosis, as well as the latest advancements in related drug research. The research indicates that cGAS converts ATP and GTP into cGAMP, activating the STING pathway, which triggers the production of type I interferons and participates in the immune response, cellular senescence, and inflammation processes in the aforementioned diseases. This article provides a reference for further understanding the pathogenesis of inflammatory pulmonary diseases and targeting therapeutic strategies, offering new perspectives for future research.
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Investigation into the visualization of cerebral collateral arteries in mice via diverse experimental approaches

TIAN Hao, WANG Li, GUAN Yubin, WEI Ying, HUANG Zheng, MA Cungen, MA Dong, SONG Lijuan

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Objective: Collateral circulation represents an endogenous anastomotic route that serves to compensate for the stenosis or occlusion of intracranial arteries. It supplies collateral blood flow, thereby sustaining the survival of the ischemic penumbra. This study aims to observe the labeling effects of different experimental methods on the cerebral collateral arteries of mice in vitro and in vivo. Methods: Primary (Willis circle) and secondary (leptomeningeal) collateral arteries in mice were labeled in vitro using latex perfusion, DiI perfusion, and ink-gelatin perfusion techniques. Subsequently, the diameter of these collateral arteries was meticulously measured. Specifically, the latex perfusion method was employed to compare the number of LMCs between different mouse strains. To enable stable in vivo observation of LMCs, a closed cranial window was successfully constructed. Additionally, a mouse model of distal middle cerebral artery occlusion stroke was established via electrocoagulation, followed by triphenyltetrazolium chloride (TTC) staining. For further investigation, the diameter of LMCs was continuously monitored using a fluorescence stereomicroscope, while the blood flow in the peri-infarct area was detected by laser speckle contrast imaging. Results: The latex perfusion method and DiI perfusion method can both label collateral artery vessels, but not veins. There is no significant difference in the diameter of collateral vessels measured by the latex perfusion method and DiI perfusion method (P > 0.05). The DiI perfusion method often exhibits suboptimal perfusion efficiency. The number of LMCs in C57BL/6 mice is significantly higher than that in Balb/C mice (P<0.0001). During the 3-week period of the closed cranial window, the clarity or imaging quality of the cranial window was not significantly affected. TTC staining shows the stable construction of the mice stroke model. The diameter of the LMCs increases and the blood flow in the peri-infarct area recovers after ischemic stroke (P<0.05). There is a strong positive correlation between them (P<0.05). Conclusions: Latex perfusion method can effectively label the primary and secondary collateral arteries of mice in vitro. Through fluorescence stereomicroscope and laser speckle contrast imaging, continuous observations can be made on LMCs in vivo. The remodeling of collateral vessels after ischemic stroke may promote the recovery of blood flow in the penumbra.
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Research Progress on Probiotics for Cancer-Related Fatigue in Postoperative Breast Cancer Patients Receiving Chemotherapy

Suriguga, NIU Luying, Cai Zhihui

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Breast cancer ranks among the most prevalent malignancies in women. Chemotherapy, a cornerstone of its multimodal treatment, frequently induces a spectrum of adverse effects, with cancer-related fatigue (CRF) being the most common and clinically impactful. Currently, the pathogenesis of CRF remains incompletely elucidated, and reliable diagnostic and therapeutic strategies are lacking. Impairment of intestinal barrier function is recognized as one of its key pathogenic mechanisms, while probiotics have been shown to alleviate fatigue symptoms by repairing the intestinal barrier and modulating immune-inflammatory responses. This review synthesizes the research progress regarding the role of probiotics in managing CRF in breast cancer patients undergoing postoperative chemotherapy, aiming to provide novel insights for clinical adjuvant therapy.
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Research progress of Gas7 in the nervous system

XU Ruike, PU Shan, LI Yunlan, HONG Shijun, YANG Genmeng

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Growth Arrest-Specific Protein 7 (Gas7), a member of the growth arrest-specific protein family, encodes a protein that is rich in α-helix structure and is highly expressed in the central nervous system, particularly in the cortex, hippocampus, and cerebellum. This review comprehensively examines the diverse functions of Gas7 in the nervous system, including its critical regulatory roles in nervous system development, neuronal differentiation and maturation, microtubule dynamics, cell cycle regulation, neuronal migration, axon guidance, neuronal mitophagy and repair, as well as synaptic plasticity. The results suggest that the abnormal expression of Gas7 is closely related to the occurrence of a variety of nervous system diseases and drug addiction. Nevertheless, the molecular regulation and underlying mechanisms of GAS7 remain to be fully elucidated. Further investigation in this area may offer novel insights into the pathogenesis of neurological diseases and serve as a theoretical foundation for the development of innovative therapeutic strategies.
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A Comparative Investigation into the Rabbit Brain Infusion and Lipopolysaccharide - Induced Diffuse Intravascular Coagulation (DIC) Model in Rabbits for Medical Laboratory Teaching

Yuliang Rao, Yadong Zhang, Yufeng Yan

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OBJECTIVE: To compare the application value of rabbit brain fluid (TF) and lipopolysaccharide (LPS)-induced disseminated intravascular coagulation (DIC) model in medical laboratory teaching. METHODS: The two classical models were systematically compared from four dimensions: pathogenic mechanism, modeling technology, detection system, and teaching application, and the research results and teaching practice were integrated. Results: The rabbit brain fluid model simulates acute traumatic DIC through exogenous coagulation activation, and the LPS model replicates chronic infectious DIC through endogenous inflammation-coagulation cascade, which complement each other in terms of pathogenicity, index characteristics, and experimental skills training. CONCLUSION: The optimization strategy of mechanism-oriented-skill stratification-clinical mapping can significantly improve students" knowledge and practical ability in the complex pathological process of DIC, and provide a three-dimensional solution for medical laboratory teaching.
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A Study of the Mechanism of Gouty Arthritis Attack Induced by Hyperuricemia under Ice-Water Swimming Conditions Based on P2X7R

CHEN Siying, WANG Yinfeng, LU Chengjin, CAI Xxiaoxiao, ZHANG Bin, LIN Zhijian

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Objective: To investigate the mechanism of gout attack in hyperuricemic rats under ice-water swimming conditions based on P2X7R. Methods: Male SD rats were randomly divided into control group, high-purine diet + ice-water swimming group, high-purine diet group, and ice-water swimming group. Hyperuricemia was induced by gavage with potassium oxonate combined with yeast. Ice-water swimming was performed by 5-minute endurance swimming in an ice-water mixture. The experiment lasted for 21 days. During the experiment, changes in the diameter of the right ankle joint and foot thickness were measured every two days to calculate the swelling index; serum uric acid levels in rats were detected by the uricase method; serum and liver xanthine oxidase (XOD) levels were detected by colorimetric method; serum ATP levels were detected by phosphomolybdic acid colorimetric method; uric acid crystals in joint fluid were observed by polarized light microscopy; serum levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were detected by enzyme-linked immunosorbent assay (ELISA); venous blood neutrophil count was detected by an automated hematology analyzer; pathological changes in ankle joint and synovial tissue were observed by HE staining; and P2X7R and NLRP3 protein expression in synovial tissue were detected by Western blot and immunohistochemistry, respectively. Results: Compared with the control group, serum uric acid levels in the high-purine diet + ice-water swimming group were significantly increased (P<0.01), and significantly higher than those in the high-purine diet group and ice-water swimming group (P<0.01 or P<0.05). Serum and liver XOD levels were significantly increased (P<0.01). The swelling index of the right ankle joint and foot thickness in the high-purine diet + ice-water swimming group was significantly increased, reaching a peak swelling on day 13 (P<0.01 or P<0.05), and inflammatory infiltration was observed in the synovial tissue. Venous blood neutrophil count was significantly increased (P<0.01), and serum inflammatory factors IL-1β, IL-6, and TNF-α levels were significantly increased (P<0.01). Serum ATP levels in the high-purine diet + ice-water swimming group showed a decreasing trend (P<0.1). Uric acid crystals were observed in joint fluid smears. P2X7R and NLRP3 protein expression in synovial tissue were significantly increased (P<0.01 or P<0.05). Conclusion: Ice-water swimming under hyperuricemic conditions can lead to ATP metabolic imbalance, promote increased uric acid levels and urate deposition, activate P2X7R, and consequently lead to gouty arthritis attack through the ATP-P2X7R-NLRP3 pathway.
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Strategies for occupational health and safety and emergency management in humans exposed to monkey B virus

Lin Danrong, Huang Manqi, Yang Jinchun, Chen Lin, Li Huiping, Deng Shaochang

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Macaques are experimental animals widely used in biomedical research. Monkey B virus (Cercopithecine Herpesvirus Type 1, BV) is a zoonotic pathogen. When it naturally infects macaques, the infection rate in macaques can be as high as 70% to 100%. BV infection in macaques usually presents as asymptomatic or mild symptoms, but once transmitted to humans, it can cause severe encephalomyelitis and neurological sequelae, with a fatality rate of over 40% for infected cases. BV can also remain latent in the human body for a long time and be reactivated under specific circumstances, leading to serious neurological diseases. Most people infected with BV are animal caregivers, veterinarians and laboratory researchers. The severity of human BV infection makes BV the main zoonotic disease problem among those in contact with macaques. At present, there is no vaccine to prevent human infection with BV, nor are there any specific antiviral drugs for BV. Therefore, implementing preventive measures through occupational health and safety management, conducting standardized emergency response to exposure incidents, and promptly blocking or reducing the invasion of BV are key strategies for lowering the risk of human BV infection and mortality. This article reviews the characteristics of human cases of BV infection, preventive measures for occupational health and safety management related to BV, emergency treatment measures after exposure, exposure risk assessment, post-exposure prophylaxis, and key points of post-exposure follow-up, with the aim of providing useful references for laboratory animal institutions and medical institutions in the practice of BV prevention and control.
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Research Progress on the Regulation of Cerebral Ischemia-Reperfusion Injury by the Nrf2/HO-1 Signaling Pathway

LIANG han, DONG zhiqiang, SHI ruili

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Cerebral Ischemia-Reperfusion Injury ( CIRI ) is a key pathological link in the deterioration of neurological function after stroke. Its mechanism is closely related to oxidative stress and inflammatory response, and ultimately leads to severe neuronal damage. In recent years, the nuclear factor E2-related factor 2 / heme oxygenase-1 ( Nrf2 / HO-1 ) signaling pathway, which mediates endogenous protective effects, has received extensive attention. This pathway plays a central role in maintaining cellular redox homeostasis by regulating antioxidant, anti-inflammatory and anti-apoptotic processes. The purpose of this paper is to explore the activation mechanism and multi-directional protective effect of Nrf2 / HO-1 signaling pathway in CIRI, and to analyze the therapeutic potential of targeting this pathway based on this, so as to provide theoretical basis for the development of new neuroprotective drugs, in order to optimize clinical treatment strategies and improve the prognosis of patients.
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Mechanistic role of the IP3R2/GRP75/VDAC1 axis in regulating mitochondrial calcium transport to promote hypoxia-Induced apoptosis in pulmonary artery smooth muscle cells

Guo Xue, Wang Rui, Liu Fengqian, Cheng Yang, Liu Wentao, Wang Lianzhi, Wu Yun

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Objective To investigate the role of the IP3R2/GRP75/VDAC1 axis in regulating mitochondrial calcium transport in apoptosis in an in vitro hypoxia-induced injury model of pulmonary artery smooth muscle cells (PASMCs). Methods Rat PASMCs were cultured in vitro and randomly divided into three groups: normal control group, hypoxia group, and a drug intervention group (4-Phenylbutyric acid). Intracellular, endoplasmic reticulum(ER), and mitochondrial Ca_²⁺ concentrations in PASMCs were measured using Ca_²⁺ fluorescent probes. Mitochondrial structure and morphological changes were observed by transmission electron microscopy. Cell apoptosis was detected by flow cytometry. The mRNA and protein expression levels of key factors in the Ca_²⁺ pathway and mitochondrial fission and fusion were determined by RT-qPCR and Western blot, respectively. Results In the hypoxia-induced injury model, the concentrations of Ca₂₊^{in the}ER and cytoplasm of PASMCs increased, while the mitochondrial Ca₂₊concentration decreased (P<0.01). Mitochondria exhibited reduced volume, swelling, disordered cristae structure, and increased rupture; PASMC apoptosis decreased (P< 0.01). The mRNA and protein expression levels of key Ca_²⁺ transport pathway factors IP3R2, GRP75, and VDAC1 were upregulated (P<0.01), as was the expression of the mitochondrial fission factor DRP1 (dynamin-related protein 1) (P<0.01), while the expression of the mitochondrial fusion factor MFN2 (mitofusin-2) was downregulated (P<0.01). After intervention with 4-PBA, compared to the hypoxia group, the concentrations of Ca₂₊^{in the}ER and cytoplasm of PASMCs decreased, while mitochondrial Ca₂₊^{concentration increased (}P<0.05). Mitochondrial structure was restored, and the expression of IP3R2, GRP75, VDAC1, and DRP1 decreased, while MFN2 expression increased, with an increase in PASMCs apoptosis. Conclusion The IP3R2/GRP75/VDAC1 axis enhances mitochondrial Ca₂₊^{transport in hypoxia-induced PASMCs,}promoting PASMCs apoptosis, and provides a theoretical basis for the prevention and treatment of HPH.
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Progress in the Application of Artificial Intelligence in Laboratory Animal Science Teaching

YUAN Xiaolong, SHAO Jiahao, WANG Tiantian, CAI Zhaowei, ZHUO Zhenjian, DU Xiaoyan

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Laboratory animal science has been established as the fundamental course in many disciplines such as clinical medicine and animal science, and artificial intelligence (AI) has been widely applied in clinical medicine and laboratory animal teaching. Here we summarize the application of AI based virtual simulation technology to assist experimental animal teaching, optimize experimental animal monitoring and analysis, and construct virtual animal models in teaching. Also, we list the domestic and international platforms as well as AI tools, and collect the advantages of AI to improve teaching efficiency. It is expected that the application of AI will not only break through the bottleneck of traditional teaching, but also will promote the integration and optimization of multiple disciplines in laboratory animal science, cultivate students’ creative thinking, and improve teaching quality.
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Research Progress on Traditional Chinese Medicine in Treating Diabetic Kidney Disease Based on the AMPK Signaling Pathway

sun yu shan, hou ya wei, pan guang hui, xiao zhen wei

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In recent years, the global incidence of diabetes mellitus has been on a steep rise, with diabetic kidney disease（DKD）, one of the most prevalent microvascular complications, emerging as the primary cause of end-stage renal disease (ESRD). DKD patients often present with comorbidities such as cardiovascular diseases, which exacerbate their clinical status and mortality risk. Consequently, there is an urgent need to identify safe, reliable, cost-effective, and low-side-effect medications for early DKD intervention to delay disease progression. Pathological studies have revealed that the adenylate-activated protein kinase (AMPK) signaling pathway plays a central role in DKD pathogenesis, offering a novel therapeutic direction by regulating inflammatory responses, oxidative stress, autophagy, apoptosis, lipid metabolism, ferroptosis, and other biological processes.The integration of the "holistic concept" and "evidence-based treatment" is a cornerstone of Traditional Chinese Medicine (TCM), which has demonstrated unique clinical advantages in DKD management. TCM has been shown to effectively alleviate edema, proteinuria, and renal function decline, while significantly improving patients' quality of life—an especially critical consideration for early DKD intervention. Current research focuses on merging TCM's holistic approach with modern medicine's precision in targeting signaling pathways for DKD therapy. Notably, terpenoids, flavonoids, phenolic compounds, alkaloids, and TCM formulations (e.g., Shuilu Dihuang Capsule, Angelica Sinensis Blood Tonic Soup, Tangshen Ning Formula, Jinlida Granule, and Torch Root Tablets) have exhibited significant targeting effects on AMPK. This review comprehensively synthesizes recent domestic and international advancements in TCM-mediated regulation of the AMPK signaling pathway in DKD.
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Research progress of traditional Chinese medicine intervention on ischemic stroke based on oxidative stress

huawenlong, limengxing, qiaofeng, jiangyuqing, sunmengjie, tangwei

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Ischemic stroke (IS) is a cerebrovascular disease with high mortality worldwide. Its occurrence and development are closely related to oxidative stress. At present, vascular recanalization is mainly used to restore cerebral blood circulation in clinical practice. However, this therapy may also cause cerebral ischemia-reperfusion injury and further aggravate neurological damage. The single-target treatment strategy of modern medicine has certain limitations, which makes the overall intervention advantages of multi-component, multi-channel and multi-target of traditional Chinese medicine increasingly valued. This paper systematically summarizes the research progress of oxidative stress involved in the pathological process of IS by mediating inflammatory response, affecting the function of neurovascular units, regulating key signaling pathways, destroying the integrity of the blood-brain barrier, inducing apoptosis and regulating autophagy. In recent years, scholars at home and abroad have carried out extensive research on traditional Chinese medicine monomers and active ingredients, traditional Chinese medicine compound and traditional Chinese patent medicine intervention, it IS confirmed that traditional Chinese medicine has good potential in improving clinical symptoms and neurological function recovery. Based on the perspective of oxidative stress, this paper aims to summarize the mechanism of action and clinical research progress of traditional Chinese medicine intervention,, so as to provide theoretical reference and research ideas for the clinical prevention and treatment of the disease and the development of new drugs. Follow-up studies should focus on elucidating the mechanism of multi-component synergistic anti-oxidative stress of traditional Chinese medicine, constructing a sequential treatment scheme of integrated traditional Chinese and Western medicine, and carrying out high-quality clinical evidence research, it provides accurate prediction models, timing optimization strategies and high-level evidence-based medical evidence for the prevention and treatment of cerebral ischemia-reperfusion injury, promotes the transformation of basic research results into clinical practice, and provides new strategies for the prevention and treatment of IS.
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Mechanistic Study of ADAM17 Regulating Endoplasmic Reticulum Stress in Cyclosporine A-Induced Renal Fibrosis in SD Rats

mengsiqi, qilongyu, gaoranran, hancong, huhongzhen, zhoule, wangyichuan, liwei

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Objective To investigate the regulatory mechanisms of a disintegrin and metalloproteinase 17 (ADAM17)?and endoplasmic reticulum stress (ERS) in cyclosporine A (CsA)-induced renal fibrosis, and to identify potential novel therapeutic targets in the progression of renal fibrosis.Methods A CsA-induced renal fibrosis model was established in SD rats via gavage. Plasmid transfection and siRNA technologies were employed to overexpress or knock down ADAM17 in vivo. Indices including body weight,urine protein/creatinine ratio (UPCR),serum blood urea nitrogen (BUN), serum creatinine (Scr), cystatin C (Cys-C),transforming growth factor-β1 (TGF-β1), and ADAM17 were measured. Pathological changes in kidney tissues were observed via hematoxylin-eosin (HE) staining and Masson's trichrome staining. Ultrastructural alterations were examined using transmission electron microscopy (TEM). Co-expression of ADAM17 and glucose-regulated protein 78 (GRP78) was detected by immunofluorescence. mRNA expressions of TGF-β1， SMAD homolog 3 (SMAD3),α-smooth muscle actin (α-SMA), collagen type I alpha 1 chain (COL1A1),ADAM17,and GRP78 in kidney tissues were analyzed via reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). Protein expressions of ADAM17,SMAD3, TGF-β1, α-SMA,COL1A1, and GRP78 were measured by Western blotting (WB).Results In the CsA-induced model group, rats exhibited decreased body weight,significantly increased UPCR,serum renal function indicators (BUN, Scr,Cys-C), serum ADAM17, and serum TGF-β1 levels (p < 0.01). Morphological examinations revealed pathological changes such as renal interstitial fibrosis. RT-qPCR showed upregulated mRNA expressions of TGF-β1,SMAD3,and ADAM17 (p < 0.01), while WB demonstrated significantly elevated protein levels of TGF-β1, SMAD3,and ADAM17 (p < 0.01). Overexpression of ADAM17 (p < 0.001) led to a marked decrease in body weight,significant increases in serum renal function indicators and UPCR (p < 0.01), and typical pathological changes including renal interstitial fibrosis. Immunofluorescence, RT-qPCR,and WB all showed increased GRP78 expression,along with abnormal upregulation of TGF-β1,SMAD3, COL1A1, α-SMA, and other indicators (p < 0.01). Conversely, knockdown of the ADAM17 gene in the model group alleviated these abnormal expressions to varying degrees (p < 0.05).Conclusions ADAM17 significantly promotes fibrosis progression, and its dysregulation of endoplasmic reticulum stress (ER stress) may serve as a critical mechanism underlying this pro-fibrotic process.
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Research Progress on the Regulation of T Lymphocytes by Traditional Chinese Medicine in the Treatment of Sj?gren

Wang Chengzhi, Li Songwei, Du Mengmeng, Li Huan

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Sjogren"s Syndrome (SS) is a chronic autoimmune disease, which usually occurs due to immune system disorders. However, the specific mechanism is still unclear and it cannot be cured. T lymphocytes are an important type of immune cells in the human body, and their role in the occurrence and development of SS has been widely described. They are an important target for anti-SS treatment. Although modern medical treatment of SS can alleviate symptoms and delay progression to some extent, it has obvious clinical limitations and the overall treatment effect is not satisfactory. It is particularly important to find an effective and safe treatment method. Traditional Chinese medicine treats diseases based on the fundamental principles of syndrome differentiation and holistic concept, and has multi-pathway, multi-level, and multi-target anti-SS effects. Studies have found that active ingredients of traditional Chinese medicine such as Fangji Noling Alkaloid, Bai Shao Total Glycosides, and Rhodiola Rhodiola Glycosides, as well as traditional Chinese medicine compound prescriptions such as Runzhuang Lingfang, Yangyin Yijieli Huoxue Fang, and Jiefu Huaxue Shengjing Fang, can regulate the changes of different T lymphocyte subsets by regulating signaling pathways such as PI3K/AKT/mTOR, STAT3, and NF-κB, and synergistically alleviate inflammatory responses, reduce immune infiltration, and improve glandular function, etc., to achieve the therapeutic effect of SS. This article reviews and analyzes the relevant research on traditional Chinese medicine against SS in recent years, and discusses the mechanism of traditional Chinese medicine regulating T lymphocytes against SS. The aim is to provide new ideas for the clinical treatment of SS.
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Research Progress on miRNA Regulating Immune Cells for the Treatment of Sjogren

Wang Chengzhi, Li Songwei, Du Mengmeng, Li Huan

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Sjogren"s Syndrome (SS) is a chronic autoimmune disease characterized by complex pathogenesis and suboptimal treatment outcomes. Its onset is closely linked to dysregulation of the immune system. As key components of this system, immune cells influence SS development by modulating lymphocyte infiltration, inflammatory responses, and epithelial cell proliferation. MicroRNAs (miRNAs) play a crucial role in regulating gene expression, thereby impacting immune responses, metabolic processes, and cellular activities, and are widely implicated in the pathogenesis, progression, and prognosis of SS. Specific miRNAs, such as miR-31-5p, miR-100-5p, and miR-125b, have been shown to target signaling pathways including p38 MAPK and JAK/STAT. Through these pathways, they modulate the function of macrophages, dendritic cells, T lymphocytes, and B lymphocytes, ultimately reducing inflammation, improving glandular function, and exerting anti-SS effects. This article reviews the current literature to discuss the specific mechanisms by which miRNAs regulate immune cells in the context of SS treatment, aiming to provide insights and references for future therapeutic strategies.
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Effect and mechanism of Yulangsan Chalcone on Ang II-induced H9c2 cardiomyocyte hypertrophy

LIANG Xingmei, NONG Huiliang, LIAO Naiying, LIU Antao, MENG Ganzhu, HUANG Renbin, ZHANG Ting, FU Peng

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Abstract:

Objective: To investigate the protective effect of Yulangsan Chalcone (YLSC) on H9c2 cardiomyocytes hypertrophy induced by angiotensin II (Ang II) and its possible mechanism. Methods: H9c2 cardiomyocytes were divided into blank control group, model group, and low-, medium-, and high-dose groups of YLSC. After intervention with YLSC, the cells were induced to form a hypertrophy injury model with Ang II at a concentration of 1 μmol/L. Cell viability was detected by CCK-8, autophagy of apoptotic substances was detected by MDC staining, ROS levels were detected by DCFH-DA fluorescence probe method, apoptosis was detected by Hoechst 33342 staining, ATP content was detected by ELISA, and the levels of Bnip-3 and Atg5 were detected by RT-PCR. The expressions of autophagy marker proteins p62, Beclin1 and LC3II/LC3I were detected by WB. Results: YLSC can alleviate Ang II-induced H9c2 cardiomyocyte hypertrophy injury. CCK-8 assay indicates that YLSC can enhance the viability of hypertrophic cardiomyocytes. MDC staining method suggests that YLSC can initiate autophagy to clear apoptotic cells. DCFH-DA fluorescence probe method detection results show that YLSC can reduce the generation of reactive oxygen species. Hoechst 33342 staining method detection results show that the test drug can reduce cell apoptosis. ELISA detection results show that the test drug can increase the ATP level of cells. RT-PCR detection results show that the test drug can promote the gene expression of Bnip-3 and Atg5. WB detection results show that YLSC can reduce the expression of p62 and increase the expression of Beclin1 and LC3II/LC3I. Conclusion: YLSC can effectively inhibit Ang II-induced H9c2 cardiomyocyte hypertrophy and apoptosis, and its mechanism may be related to the initiation of myocardial autophagy, activation of autophagy-related factors and clearance of apoptotic cells.
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Construction and Operation Practice of Laboratory Animal Facilities in Hospital

zuopeipei

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【】 Experimental animal facilities play a very important role in hospital scientific research work. Their construction standards and specifications, design principles and functional layout, equipment configuration and environmental control, as well as operation management, quality control, safety management, personnel training and other aspects should all follow unified standards and requirements. However, due to the complex and systematic nature of the construction of experimental animal facilities, each research institution and hospital has significant differences in the design concept, purpose, geographical location, construction requirements, personnel composition and other aspects of the facilities. In the specific construction and operation practice of experimental animal facilities, the problems encountered are also different. This article discusses the construction and operation of experimental animal facilities at the Central China Branch of the National Cardiovascular Disease Center, summarizes the experience of our unit in the construction and operation of experimental animal facilities, and provides theoretical guidance and practical reference for the construction and operation of experimental animal facilities in the hospital system.
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Research Progress on Primary Culture and Identification of Penile Cavernous Cell

yemiaoyong, zhangjie, zhaofan

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The primary cell isolation and culture of penile corpus cavernosum is one of the key technical methods for studying the pathological mechanisms of erectile dysfunction (ED). This review provides a detailed summary of the isolation and culture methods for major cell types in the penile corpus cavernosum, including smooth muscle cells (CSMCs), endothelial cells (CECs), pericytes (CPs), and fibroblasts (CFs). Commonly used techniques such as enzymatic digestion, tissue explantation, immunomagnetic bead separation, and Matrigel induction are discussed, with a comparative analysis of their advantages and disadvantages. Additionally, methods for the identification of different cell types are summarized. This systematic review of cell culture and identification techniques offers certain technical support and reference for further research into the roles of penile corpus cavernosum cells in the onset, progression, and treatment of ED.
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Research Advances in Macrophage Iron Metabolism in Acute Kidney Injury

Wang Jin Zheng, Yang Lawei, Pan Qingjun

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Acute Kidney Injury is a common clinical syndrome characterized by a rapid decline in renal function over a short period, accompanied by abnormal urine output, azotemia, and other symptoms. The pathological mechanisms of AKI are highly complex, primarily involving inflammatory responses, oxidative stress, and cell death processes. In recent years, the incidence of AKI has continued to rise, particularly among critically ill patients, making it an urgent global public health challenge. Emerging studies suggest that macrophages play a dual role in the progression and recovery of AKI through dynamic regulation of iron metabolism. This article systematically elaborates the mechanisms by which imbalanced macrophage iron metabolism impacts AKI: iron overload exacerbates inflammation by inducing M1 polarization, promoting lipid peroxidation and ferroptosis, whereas iron restriction may enhance antioxidant capacity via activation of pathways such as Nrf2, driving M2 polarization to facilitate tissue repair. These findings provide novel insights into the pathogenesis of AKI and establish a theoretical foundation for developing new therapeutic targets and strategies.
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Research Progress on the Treatment of Substance Use Disorders with Repetitive Transcranial Magnetic Stimulation

TAO Huishan, RAO Mengjie, TIAN Yunqing, WANG Chan, LIU Liu, ZENG Xiaofeng

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The abuse of addictive substances will lead to a series of legal and public health problems, causing great harm to individuals, families and society. Addictive substances cause behavioral changes and cognitive dysfunction by affecting the release of neurotransmitters and changes in neuroplasticity in the brain. Repetitive transcranial magnetic stimulation is a non-invasive neuromodulation method for treating substance use disorders, which can improve the craving behavior and cognitive impairment of patients with substance use disorders. This article systematically reviews the great potential of repetitive transcranial magnetic stimulation in the treatment of substance use disorders by reviewing the research results of repetitive transcranial magnetic stimulation in the treatment of common substance use disorders in recent years, in order to provide new ideas for the treatment of substance use disorders.
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Caveolin-1 regulates iron homeostasis through the NCOA4-FTH1 pathway and slows down hepatocyte senescence in MAFLD

sunyuquan, xuhanlin, genqianqian, wangyong, liyu, wushuai, wangxingyu, guoning, huchenmu

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Objective To investigate the role of Caveolin-1 (CAV1) in the progression of metabolic-associated fatty liver disease (MAFLD) and its potential mechanisms of action. Methods Based on the human database GSE126848, we identified differential CAV1 expression in normal, obese, and non-alcoholic fatty liver disease (NAFLD) individuals. A CAV1 knockout (CAV1 KO) MAFLD mouse model was established using a 16-week high-fat diet (HFD). Albumin (ALB) and CAV1 co-localization was used to determine CAV1 expression in the liver. CAV1 mRNA and protein levels were detected in primary hepatocytes. Lipid deposition and inflammation were assessed using HE staining, Oil Red O staining, and Nile Red staining. Mitochondrial damage was observed by transmission electron microscopy. Cellular senescence and iron metabolism changes were evaluated by immunohistochemistry for cyclin-dependent kinase inhibitor 1A (P21), dihydroethidium (DHE) staining, and iron staining. Furthermore, a hepatocyte senescence model was constructed and divided into normal, palmitic acid (PA), CAV1-siRNA, and CAV1-GV146 (CAV1 overexpression) groups to analyze lipid deposition, senescence, and Fe2+ levels. Western blot, qRT-PCR, and mitochondrial membrane potential (JC-1) assays were used to further validate the effect of CAV1 on hepatocyte senescence and mitochondrial function. Results In vivo experiments showed that CAV1 KO exacerbated lipid deposition, inflammation, and liver senescence. This was evidenced by enhanced lipid staining, increased levels of senescence markers including histone H2A variant X phosphorylation (γ-H2AX), cyclin-dependent kinase inhibitor 2A (P16), and P21, decreased levels of oxidative stress markers glutathione (GSH) and superoxide dismutase (SOD), increased malondialdehyde (MDA) and reactive oxygen species (ROS), and mitochondrial shrinkage with increased mitochondrial membrane density. Iron metabolism analysis revealed that CAV1 KO led to decreased Fe3+ and increased Fe2+ accumulation, which was associated with the nuclear receptor coactivator 4-ferritin heavy chain 1 (NCOA4-FTH1) pathway. Supplementation with the CAV1 scaffolding domain (CSD) significantly improved the reduction of Fe3+ and the accumulation of Fe2+. In vitro, silencing CAV1 promoted lipid accumulation, mitochondrial damage, and cellular senescence. This was accompanied by elevated ROS levels, Fe2+ accumulation, decreased NCOA4 expression, and increased FTH1 expression. Conversely, CAV1 overexpression attenuated these effects. Immunofluorescence revealed that CAV1 silencing enhanced NCOA4 and FTH1 co-localization, an effect reversed by CAV1 overexpression. Importantly, deferoxamine (DFO) treatment reduced ROS levels and ameliorated senescence induced by CAV1 silencing. Collectively, these results indicate that CAV1 modulates liver senescence, potentially via the NCOA4-FTH1 pathway. Conclusion Caveolin-1 can slow down MAFLD hepatocyte senescence, possibly by regulating iron homeostasis through the NCOA4-FTH1 pathway.
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Effect of pinocembrin on apoptosis and migration of melanoma cells by down-regulating DAAM2/Wnt/β-catenin signaling axis

Liao yuan, Wang yu, Jia longhao, Lin jingyi, wangli

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Abstract: Objective To investigate the effect of Pinocembrin (Pin) on apoptosis and migration of mouse melanoma B16 cells and its relationship with DAAM2/Wnt/β-catenin, signaling axis. Methods CCK8 method was used to screen the Chinese medicine monomers which could inhibit the viability of B16 cells in vitro. Flow cytometry and wound healing assay were used to detect the apoptosis and migration of melanoma B16 cells. RNA-seq sequencing combined with GEPIA database was used to analyze the possible core genes of Pin. The expression levels of DAAM2 and Wnt/β-catenin signaling pathway-related proteins Axin2, p-GSK3β, and p-β-catenin were detected by real-time fluorescence quantitative PCR and Western blot. Reversion experiments were performed by transfection of a DAAM2 overexpression plasmid. A mouse melanoma model was established in vivo, and the mice were treated with low and high doses (10 mg/kg, 30 mg/kg) of Pin by gavage. The growth of melanoma in mice was observed. Western blot was used to detect the effect of Pin on the expression of DAAM2, Axin2, β-catenin and p-GSK3β in melanoma tissues to further clarify the effect of Pin on the progression of melanoma in mice. Results Pin significantly promoted the apoptosis of B16 cells (p < 0.001) and inhibited the migration of B16 cells (p < 0.01, p < 0.001). RNA-seq and GEPIA analysis suggested that DAAM2 was a key target. The results of qPCR and Western blot showed that Pin could significantly reduce the mRNA and protein expression of DAAM2 (p < 0.05, p < 0.01, p < 0.001). The expression levels of Wnt/β-catenin signaling pathway-related proteins p-GSK3β, p-β-catenin and Axin2 were down-regulated (p < 0.001). In vivo experiments showed that high-dose Pin could significantly inhibit the growth and weight of melanoma in mice, and reduce the expression of DAAM2, Axin2, β-catenin and p-GSK3β(p < 0.05, p < 0.01) in tumor tissues. DAAM2 overexpression can reverse the effect of Pin on the DAAM2/Wnt/β-catenin signaling axis. Conclusion Pin can promote the apoptosis of melanoma cells, inhibit their migration, and inhibit the growth of melanoma in mice by down-regulating the DAAM2/Wnt/β-catenin signaling axis. Key words: Pinocembrin; Melanoma; Anti-tumor; DAAM2; Wnt/β-catenin
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The mechanical response characteristics of thrombospondin-4 in vascular smooth muscle cells

Xu Fei, Zhang Jiangtao, Chai Shoudong

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Objective: To explore the dose-time dependent relationship of shear stress and different exposure times on the expression of thrombospondin-4 (THBS4) in human aortic smooth muscle cells (HASMCs), and to reveal its potential mechanism in vascular remodeling, with the aim of guiding the treatment of clinical cardiovascular diseases. Methods: HASMCs were subjected to shear stress of 0 dyn/cm2、4 dyn/cm2, 8 dyn/cm2, and 12 dyn/cm2 using a parallel plate flow chamber for 6 hours and 12 hours, respectively. Cells were collected after the treatment. The mRNA expression of THBS4 was detected by real-time fluorescence quantitative PCR, and the protein expression was detected by Western Blot. Immunofluorescence staining was performed to determine the co-localization of THBS4 and cleaved- Caspase 8. Results: The mRNA and protein expression of THBS4 gradually increased with the increase of shear stress and the extension of time. The expression levels of the gene and protein in the 12 dyn/cm2 group were significantly higher than those in the 0 dyn/cm2, 4 dyn/cm2, and 8 dyn/cm2 groups. The immunofluorescence results demonstrated that the expression of THBS4 was co-localized with cleaved- Caspase 8 and exhibited consistent expression levels. Conclusion: The spatiotemporal gradient changes of shear stress can regulate the expression of THBS4 in HASMCs, and its expression level is positively correlated with the magnitude of shear stress and has a time-dependent cumulative effect. THBS4 may modulate apoptotic pathways in HASMCs under shear stress.
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Homocysteine regulates FOXO3a to mediate mitochondrial damage in metabolism-associated fatty liver disease

JIAO Yun, ZHANG Jie, LIU Huijuan, YANG Jiaqi, WANG Yajing, LIU Honglin, MA Fang, LI Guizhong, JIANG Yideng

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Objective? To investigate the effect and mechanism of homocysteine (Hcy) regulated Forkhead box O3a (FOXO3a) -mediated mitochondrial damage in metabolic associated fatty liver disease (MAFLD).? Methods?Six weeks old Cbs+/- mice (n=12) were randomly divided into 2 groups: normal diet for 12 weeks (ND，n=6) and high methionine diet for 12 weeks (HMD，n=6).Cell Counting Kit-8 Kit was used to detect the inhibition ratio of hepatocytes treated with different concentrations of Hcy (0, 50, 100, 150 μmol/L). NCTC1469 mice normal hepatocytes were divided into Control group (Control) and Hcy intervention group (Hcy, 100 μmol/L Hcy)，NC siRNA-transfected control group (si-NC) and FOXO3a siRNA-transfected group （si-FOXO3a），NC siRNA-transfected with Hcy intervention group （Hcy+si-NC） and FOXO3a siRNA-transfected with Hcy intervention group （Hcy+si-FOXO3a）. HE staining was used to observe liver tissue injury. Oil red O was used to observe the distribution and accumulation degree of lipid droplets in hepatocytes. Total cholesterol (TC) and triglycerides (TG) were used to analyze the contents of lipid metabolites in cells. Western blot was used to detect the differences in FOXO3a protein expression in mouse liver tissues (ND and HMD) and liver cells (Control and Hcy ). ROS was used to observe the degree of oxidative stress in cells. JC-1 was used to detect the mitochondrial membrane potential. Mito-tracker was used to observe the morphological changes of mitochondria. qRT-PCR was used to detect the change of mtDNA expression in each group.? Results? Compared with ND, the structure of liver tissue in HMD was disordered, the hepatocytes were enlarged, the cytoplasm was loose and light stained, and a large number of vacuoles and lipid droplets were observed in the liver cells. Compared with the Control, the number of oil red O positive lipid droplets in the Hcy was increased, and the levels of TC and TG were increased. Compared with the ND and the Control, the expression of FOXO3a protein in the HMD and the Hcy was significantly increased. Compared with the Hcy+si-FOXO3a, the Hcy+si-FOXO3a had decreased intracellular ROS level, significantly decreased JC-1 monomer, decreased mitochondrial fragmentation, decreased number of oil red O-positive lipid droplets, and decreased TC and TG levels. ?Conclusion? FOXO3a plays an important promoting role in lipid metabolic disorders of MAFLD caused by Hcy by regulating mitochondrial damage.
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The mechanism of colitis alleviation by inhibiting the NF-κB pathway and macrophage M1 polarization via Kangfuxin Liquid in IBD mice

chenli, lijie, zhangshanshan, wangning, wuxuedong

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Objective Based on the close association between the pathological mechanism of inflammatory bowel disease (IBD) and the overactivation of the nuclear factor κB (NF-κB) signaling pathway and M1 polarization of macrophages, this study uses Kangfuxin Solution to conduct a comparative study exploring the regulatory mechanism of the NF-κB pathway during the progression of IBD. Methods A mouse model of inflammatory bowel disease (IBD) was established by inducing with dextran sodium sulfate (DSS). Forty-eight C57BL/6 mice were divided into eight groups: the control group, the model group, the sulfasalazine group (SASP), different-dose Kangfuxin Liquid groups (5, 10, 20 mL/kg), the NF-κB inhibitor pretreatment group, and the NF-κB inhibitor pretreatment + KFX-H group. The disease activity index (DAI), colonic mucosal damage index (CMDI), histopathological scores were recorded, the mRNA expression levels of CD86, tumor necrosis factor-α (TNF-α), phosphorylated IκBα (p-IκBα) and IL-1β in colonic tissues were detected by fluorescence quantitative PCR, and protein expression levels of CD86, iNOS, and phosphorylated IκBα (p-IκBα) in colon tissues by protein blotting (Western Blot). Flow cytometry was used to analyze the effect of Kangfuxin liquid on the disease model. The detection results were compared and analyzed among groups. Results The DSS-induced method successfully established a mouse IBD model, with the measured values of various research indicators being the highest in the model group (P<0.05). After drug intervention, except for the sulfasalazine group in which the downregulation of CD86 was relatively small and the difference compared with the model group was not statistically significant (P>0.05), the indicators in each group were significantly decreased compared with those in the model group (P<0.05). Among the three groups intervened with Kangfuxin Liquid, the high-dose group showed a significant downregulation of indicators (P<0.05). However, the combined intervention of NF-κB inhibitor and high-dose Kangfuxin Liquid did not significantly enhance the therapeutic effect, and the differences in the measured values of each indicator compared with those in the groups with single-drug intervention were not statistically significant (P>0.05). Conclusion NF-κB inhibitors, sulfasalazine, and Kangfuxin liquid all have protective effects on colonic inflammation in DSS-induced IBD model mice, but their sites of action differ. NF-κB inhibitors and Kangfuxin liquid are synergistic in attenuating the intestinal inflammatory response by inhibiting NF-κB pathway activation through lowering the level of IκBα phosphorylation, as well as down-regulating macrophage M1-type polarization.
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Research progress on central biological changes in animal models of liver depression syndrome and the regulatory mechanism of traditional Chinese medicine

KUANG luoyi, LUO zilong, JIA qing, WANG minzhi, YANG tiezhu, CHEN yulong, WU yaosong, LIU yan

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Liver depression syndrome (LDS) is commonly observed in various clinical diseases. Extensive studies have demonstrated that chronic stress serves as the primary trigger for LDS, and its biological mechanisms closely related to the changes in the morphology and function of multiple central brain regions. However, the relevant evidence remains scattered across numerous studies, necessitating further synthesis and review. Based on this, this paper reviews the animal modeling and evaluation methods of LDS, the relationship between LDS pathogenesis and morphological, functional, and molecular changes in brain regions such as the hippocampus, cortex, hypothalamus, locus coeruleus, striatum, and amygdala, as well as the regulatory effects of traditional Chinese medicine (TCM). The findings provide a foundation and direction for further research into the biological basis of LDS, the identification of syndrome-specific targets, and the exploration of therapeutic mechanisms of TCM compounds.
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Effect of Xingnao Kaiqiao acupuncture on depressive behavior in post-stroke depressed rats by adjusting P2X7R/NLRP3/IL-1β pathway

Jin yu

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Objective: To explore the effect of Xingnao Kaiqiao acupuncture on depressive behavior in post-stroke depressed rats by adjusting P2X7 purinergic receptor (P2X7R)/NOD-like receptor family pyrin domain containing 3 (NLRP3)/interleukin-1β (IL-1β) pathway. Methods: A post-stroke depression model rat was constructed and grouped into a model group, a positive control group (fluoxetine group), an acupuncture group, a pathway inhibitor group (CBBG group), and an acupuncture+pathway activator group (acupuncture+BzATP group). Healthy rats were included as the control group. The depression like behavior (sugar preference test, open field test), serum inflammatory and oxidative stress factors (ELISA method), pathological changes in hippocampal tissue (HE staining, Nissl body staining), neuronal apoptosis in hippocampal tissue (TUNEL method), and the P2X7R, NLRP3, IL-1β, Iba-1, Bcl-2, Bax, and cleaved caspase3 proteins in hippocampal tissue (Western blot method) were detected. Results: For the control group, the model group showed a clear decrease in glucose preference and open field activity distance in rats, clear pathological damage to brain tissue, a clear increase in serum inflammatory factors, MDA, and proportion of neuronal apoptosis, a clear decrease in CAT activity, a clear increase in P2X7R/NLRP3/IL-1β pathway proteins, Iba-1, and pro apoptotic proteins in hippocampal tissue, and a clear decrease in anti apoptotic proteins (P<0.05). For the model group, the fluoxetine, acupuncture, and CBBG groups showed an increase in glucose preference and open field activity distance in rats, reduced pathological damage in hippocampal tissue, increased number of Nissl bodies, a decrease in serum inflammatory factors, MDA, and proportion of neuronal apoptosis, an increase in CAT activity, a decrease in P2X7R/NLRP3/IL-1β pathway proteins, Iba-1, and pro apoptotic proteins in hippocampal tissue, and an increase in anti apoptotic proteins (P<0.05). For the acupuncture group, the acupuncture+BzATP group showed showed aggravated depressive behavior, clear pathological damage to hippocampal tissue, and a decrease in the number of Nissl bodies in rats, the inflammation and oxidative stress reactions occurred in the body, the P2X7R/NLRP3/IL-1β pathway proteins, Iba-1, and pro apoptotic proteins increased, while the anti apoptotic proteins decreased (P<0.05). Conclusion: The Xingnao Kaiqiao acupuncture may alleviate inflammation and oxidative stress response, inhibit neuronal apoptosis in rats by adjusting P2X7R/NLRP3/IL-1β pathway, thereby improving hippocampal tissue damage and exerting antidepressant effects.
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Comparative study of water content calculation methods in mouse plateau cerebral edema / pulmonary edema model

zhangzihui, weixu, 黄蕊, hemin, xiaopan, niutingxian, shendongshuai, chenkeming

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【Abstract】Objective: To develop mouse brain / pulmonary edema model under different conditions to calculate water content and make a comparative study. Methods: 50 male BALB / c mice were randomly divided into control and 4 experimental groups: 6000 m / 48 h, 6000 m / 72 h, 8000 m / 48 h, 8000 m / 72 h, 10 in each group. The precursor mass of each group of mice was recorded. Except for the blank group, the other groups were placed in the simulated plateau environment at the altitude of 6000m or 8000m, exposed for 48 h or 72 h, and the blank group was not treated. After the exposure time, the body mass was weighed, and the lung wet weight, brain wet weight, lung dry weight and brain stem weight were collected and calculated. Three different calculation methods were used to calculate the model water content and conduct differential analysis, and the pathological changes of brain and lung were observed by HE staining. Results :Except for the blank group, the body mass of mice in all experimental groups decreased significantly (P <0.01), and the body mass decreased most significantly after 72 h at the same altitude. Analysis of the pulmonary edema model: in the 6000 m / 48 h group, Not significantly different from the blank control group (P> 0.05), Pathological analysis showed slight pulmonary edema in the 6000 m / 48 h group; The calculation results of method 2 or method 3,6000 m / 72 h, 8000 m / 48 h, 8000 m / 72 h, Are significantly higher than the blank control group (P <0.01), Meanwhile, pathological analysis indicated significant edema in the lungs of these 3 groups, However, the lung water content of these three groups was not significantly different from the blank control group as calculated by method 1 (P> 0.05). Analysis of cerebral edema model: when calculated by method 1, the brain water content of each experimental group was significantly lower than that of the blank control group (P <0.01); the calculation results of method 2 and 3 were completely consistent, and the brain water content of each experimental group was significantly higher than that of the blank control group (P <0.01); the pathological analysis showed that the brain of the four experimental groups had significant edema. Conclusion: Method 1 has a more serious error. Methods 2 and 3 have similar calculation results, which both introduce the ability to correct body mass changes, and are recommended as the standard calculation method for the plateau brain / lung edema model.
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Study on the mechanism of the Formula for Bushen Wenyang Huayu Decoctionin regulating Notch1/ Twist1-mediated Epithelial-mesenchymal transition in the treatment of endometriosis

JIA ZE QI, XIN YU YANG, LI MEI ZHANG, XIN MENG, YI MING MA, HUI MIN LIU, JING WEI CHEN

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(1.Hebei Key Laboratory of Integrative Medicine on Liver-Kidney Patterns, Institute of Integrative Medicine, Hebei university of Chinese Medicine ,Shijiazhuang, Hebei 050091；2.Hebei Collaborative Innovation Center of Integrated Traditional and Western Medicine on Reproductive Disease,Shijiazhuang, Hebei 050091):Objective:To explore the mechanism of the Bushen Wenyang Huayu Formula in regulating the Notch1/Twist1 signaling pathway-mediated epithelial-mesenchymal transition (EMT) in the treatment of endometriosis (EMs).Methods:After modeling, the weight,volume and adhesion degree of ectopic lesions were observed; the levels of sex hormones in serum were determined by ELISA;the expressions of E-cadherin, N-cadherin, Vimentin,Notch1 and Twist1 proteins were detected by immunohistochemistry and Western blot; the expressions of E-cadherin,N-cadherin, Vimentin, Notch1 and Twist1 were detected by Real-Time PCR. Results:Compared with the sham operation group,the levels of E₂, P, FSH and LH in the serum of the model group were significantly increased(P<0.05),and the levels of N-cadherin, Vimentin, Notch1 and Twist1 proteins and mRNAs in the uterine tissue were significantly increased(P<0.01,P<0.05),while the levels of E-cadherin protein and mRNA were significantly decreased(P<0.01).Compared with the model group, the volume of ectopic lesions in the high and low dose groups of traditional Chinese medicine and the western medicine group was significantly reduced(P<0.05,P<0.01),the levels of E_2, P, FSH and LH were significantly increased(P<0.05),and the levels of N-cadherin, Vimentin, Notch1 and Twist1 proteins and mRNAs in the uterine and ectopic lesion tissues were significantly decreased(P<0.01,P<0.05), while the levels of E-cadherin protein and mRNA were significantly increased(P<0.01). Conclusion: The Bushen Wenyang Huayu Formula can significantly inhibit the progression of EMs, and its mechanism may be related to the down-regulation of the expression of the Notch1/Twist1 signaling pathway, thereby regulating the EMT process of EMs.
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Exploring the effect and mechanism of quercetin on peritoneal fibrosis in peritoneal dialysis rats based on the Wnt/β-catenin pathway

SI Shuangshuang, SUN Yuanbo, WANG Lili, LI Yu, CHEN Bowen, LI Yue

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Objective: To explore the effect and mechanism of quercetin (quercetin, QCT) on peritoneal fibrosis (peritoneal fibrosis, PF) in peritoneal dialysis (peritoneal dialysis，PD) rats based on the Wnt/β-catenin pathway. Methods: A PD rat model was constructed, and successfully modeled rats were stochastically classified into PD group, QCT-L group, QCT-H group (gavage of 17.5 mg/kg, 35 mg/kg QCT), and QCT-H+LiCl group (gavage of 35 mg/kg QCT+intraperitoneal injection of 60 mg/kg Wnt/β-catenin signaling pathway activator LiCl). Another 12 rats were stochastically served as the Ctrl group. The Ctrl group and PD group were given an equal amount of physiological saline by gavage once a day for 4 weeks. The peritoneal balance test was used to assess peritoneal function. HE staining was performed to observe changes in peritoneal tissue. Masson staining was performed to observe peritoneal tissue fibrosis. ELISA method was performed to measure inflammatory factors (TNF-α, IL-1β, IL-6). IHC was used to detect the α-SMA, CoL-1, and E-cadherin proteins in rats. Western blot was performed to detect the Wnt3a, LRP5, LEF-1, GSK-3β and β-catenin proteins in rats. Results: Compared with the 0 mg/kg LiCl group, the 30 and 60 mg/kg LiCl groups showed no significant effects on renal and peritoneal functions (P>0.05), the levels of Scr, BUN, and MTG In the 90 mg/kg LiCl group significantly increased, while UF significantly decreased (P<0.05). In addition, the 30 mg/kg LiCl group exhibited no significant impact on Wnt3a, β-catenin protein expression (P>0.05), whereas the 60 and 90 mg/kg LiCl groups showed significant upregulation of Wnt3a and β-catenin protein expression (P<0.05). Therefore, 60 mg/kg was selected as the concentration of LiCl for activating the Wnt/β-catenin signaling pathway. Compared with the Ctrl group, the peritoneal mesothelial cells of rats in the PD group shed, with a large amount of collagen fiber deposition and prominent infiltration of inflammatory cells. The serum Scr, BUN levels, MTG, peritoneal thickness, peritoneal tissue TNF-α, IL-1β, IL-6 levels, α-SMA, CoL-1, Wnt3a, LRP5, LEF-1, β-catenin proteins increased (P<0.05), while UF, E-cadherin and GSK-3β protein decreased (P<0.05). Compared with the PD group, the QCT-L and QCT-H groups showed a small amount of mesothelial cell shedding, reduced collagen fiber deposition, and infiltration of inflammatory cells in the peritoneal tissue. The serum Scr, BUN levels, MTG, peritoneal thickness, peritoneal tissue TNF-α, IL-1β, IL-6 levels, α-SMA, CoL-1, Wnt3a, LRP5, LEF-1, β-catenin proteins decreased (P<0.05), while UF, E-cadherin, and GSK-3β protein increased (P<0.05). Compared with the QCT-H group, the QCT-H+LiCl group showed a prominently increased degree of peritoneal tissue damage. The serum Scr, BUN levels, MTG, peritoneal thickness, peritoneal tissue TNF-α, IL-1β, IL-6 levels, α-SMA, CoL-1, Wnt3a, LRP5, LEF-1, β-catenin proteins increased (P<0.05), while UF, E-cadherin and GSK-3β protein decreased (P<0.05). Conclusion: QCT alleviates PF in PD rats by inhibiting inflammatory response and peritoneal mesothelial cell mesenchymal transition process, and its mechanism of action may be related to the inhibition of Wnt/β-catenin signaling pathway.
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The mechanism of Bushen Zhuanggu Decoction regulating Nrf2 / HO-1 signaling pathway to inhibit ferroptosis and improve diabetic osteoporosis model

Wei Mengjuan, Zhang Yufei, Wang Chen, Wang Yan, Wang Jingwu, Huang Chengcheng

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Objective : Through the comprehensive strategy of LC / MS analysis technology and network pharmacology, combined with experimental verification, the effective components and mechanism of Bushen Zhuanggu Decoction in the treatment of diabetic osteoporosis were discussed. Methods : UPLC-Q-Orbitrap-MS method was used to analyze and identify the effective chemical components in Bushen Zhuanggu Decoction. The genes related to DOP and ferroptosis in the database were retrieved, and the intersection was obtained to obtain the potential targets of active ingredients for the treatment of DOP by regulating ferroptosis pathway. DOP rat model was induced by intraperitoneal injection of streptozotocin combined with high-sugar and high-fat feeding. After the model was successfully constructed, Bushen Zhuanggu Decoction was administered for 8 weeks. Body weight, blood glucose and glycosylated hemoglobin were measured. Micro-CT was performed to obtain bone morphological changes. Iron ion levels, SOD and MDA levels were detected by kits. Western blot was used to detect the expression of Nrf2 / HO-1 signal and ferroptosis-related protein in bone tissue. Results : 1.A total of 848 targets of 46 identified compounds were predicted in the blood compounds of Bushen Zhuanggu Decoction. By comparing GeneCards, CTD database and FerrDb database, 81 potential targets of Bushen Zhuanggu Decoction against DOP by regulating ferroptosis were finally obtained. PPI network analysis of SIRT1, MTOR, STAT3, NFE2L2, SRC, EGFR, IL6, MAPK3, IL1B, PPARG, ALB and other nodes may be important targets for Bushen Zhuanggu Decoction in the treatment of DOP. Through KEGG pathway enrichment analysis, 134 signaling pathways about intersection target genes were obtained. The main pathways were metabolic pathways, lipid and atherosclerosis, ferroptosis signaling pathways in diabetic complications, etc. The results of in vivo experiments showed that compared with the normal group, the body weight of rats in the model group increased slowly, the levels of blood glucose and glycosylated hemoglobin increased, the trabecular bone was destroyed, the bone mineral density, bone volume fraction, trabecular thickness and density decreased, the degree of trabecular separation increased, the levels of iron ions and MDA in bone tissue increased, the activity of SOD decreased, and the expression of Nrf2, HO-1 and ferroptosis-related proteins increased ; Compared with the model group, the weight gain of rats increased, the levels of blood glucose and glycosylated hemoglobin decreased, the destruction of bone trabecula decreased, the bone mineral density, bone volume fraction, bone trabecula thickness and density increased, the separation of bone trabecula decreased, the levels of iron ions and MDA in bone tissue decreased, the activity of SOD increased, and the expression of Nrf2, HO-1 and ferroptosis-related proteins decreased. Conclusion : Bushen Zhuanggu Decoction has the characteristics of multi-component, multi-target and multi-pathway in the treatment of T2DOP. The results of in vivo experiments show that Bushen Zhuanggu Decoction can prevent and treat DOP by regulating Nrf2 / HO-1 signaling pathway and inhibiting oxidative stress and ferroptosis.
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Application of project-driven teaching guided by outcome-based education (OBE) concept in animal experiment courses

Luo Tao, Chen Liling, Chen Changlian, Hu Haisheng, Ai Zhifu, Li Shanshan

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Animal experiment courses are a crucial practical component in the life sciences field. However, traditional teaching often overemphasizes theoretical instruction, leading to issues such as insufficient skill development, weak ethical and safety awareness, detachment from real-world applications, and a lack of innovation training. To address these challenges, this study introduces the outcome-based education (OBE) concept, constructing a student-ability-centered animal experimentation curriculum system. Based on OBE, three-dimensional objectives were established: mastering foundational knowledge, proficiency in experimental skills, and enhancing comprehensive qualities. A closed-loop framework of "content conception—program design—process implementation—experience summarization" was adopted. Using authentic research projects as the vehicle, theoretical knowledge, practical skills, and research capability cultivation were organically integrated through project database construction, process-oriented evaluation, and team collaboration models. Practice demonstrates that the OBE model significantly enhanced students" knowledge mastery, skill proficiency, and teaching satisfaction, effectively fostering their team collaboration, problem-solving, and innovative thinking abilities. This study shows that project-driven teaching under the OBE concept can resolve the structural dilemmas of traditional experimental teaching, thus providing an effective pathway for enhancing the quality of animal experimentation courses and cultivating high-caliber scientific research talent.
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Potential Mechanisms Underlying the Role of the Striatum in Exercise-Mediated Improvement of Autism Spectrum Disorder

Xueyaqi, zhangshuai, made, bayi, liuniu, Zhen zhiping

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The global incidence rate of autism spectrum disorder (ASD) shows a significant upward trend. Its pathological mechanism analysis and intervention strategy development have become a major challenge in the field of neurodevelopmental disorders. Exercise intervention can significantly alleviate social disorders, cognitive deficits, and stereotyped behaviors in ASD patients, but its neurobiological mechanisms still need to be systematically elucidated. Based on the pivotal role of the striatum in the cortical basal ganglia loop and its close association with ASD behavioral phenotype and functional abnormalities, this study focuses on the key mediating role of striatal functional remodeling in exercise intervention. Through the integration of animal experiments and clinical research evidence, it has been found that the striatum plays a potential role in improving autism behavior through exercise, including strengthening the morphological structure of striatal brain regions, improving the expression of striatal neurotrophic factors, regulating the transmission of dopamine signals in striatal brain regions, enhancing the transmission of cortical striatal glutamatergic signals, and other possible mechanisms by which exercise improves striatal function. By exploring the potential role of the striatum in improving autism behavior through exercise, this multi-scale analysis framework aims to elucidate the potential role of "motor striatal functional remodeling ASD behavior improvement" and provide new ideas for exercise in improving autism behavior.
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Osteoking regulates AGEs-RAGE pathway to inhibit ferroptosis and improve knee osteoarthritis

WANG PeiJin, LI Rong, LI JinTao, JIAO JianLin, CAI Qi, ZHENG Hong

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Objective To explore the mechanism by which osteoking (OK) regulates ferroptosis and improves osteoarthritis. Method: Perform KEGG pathway enrichment analysis by analyzing target genes related to OK, OA, and ferroptosis through network pharmacology. In vivo experiments were conducted using medial meniscus instability surgery to construct a rat model of knee osteoarthritis (KOA). A sham surgery group (sham group), a model group (DMM), and osteoking group (OK) were set up, and corresponding drugs were administered orally for 8 weeks according to the grouping. Record the paw contraction reaction time (s) and weight (g) of each group of rats using a hot plate apparatus and a pressure pain gauge, respectively. ELISA kit was used to detect serum inflammatory factors TNF-α, VEGF, IL-6 and oxidative stress factors MDA, SOD, GSH, ROS in rats. Stain the knee joints of rats with eosin hematoxylin, safranin turquoise, and toluidine blue, and score the degree of cartilage tissue degeneration according to the OARSI standard. Western blot was used to detect the expression of extracellular matrix degradation protein 13(MMP13), cartilage matrix synthesis protein 2 (COLA2), glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC), advanced glycation end products (AGE), and their receptor (RAGE) proteins in rat cartilage. Using 10 mg/L IL-1β to induce human C28/I2 cells to simulate an in vitro model of arthritis, the cells were divided into control group, model group (IL-1β), OK group, and OK+AGEs group.ELISA kit was used to detect the inflammatory factor IL-6 and oxidative stress factors MDA, SOD, and GSH in the cell supernatant. Cell specific Fe2+assay kit was used to detect the content of each group of cells. Western blot was used to detect MMP13, COLA2, GPX4, and SLC11 proteins. Results The network pharmacology analysis revealed that AGE-RAGE signaling pathway and other pathways may be key pathways for OK to act on osteoarthritis and ferroptosis. In animal experiments, the model group rats showed significant increases in tenderness (P<0.01), thermal pain value (P<0.01), and OARSI score (P<0.001), as well as damage to the cartilage surface and cartilage matrix of the knee joint. Compared with the model group, OK significantly reduced tenderness, thermal pain, and OARSI scores in rats (P<0.01), alleviating damage to the cartilage surface and cartilage matrix of the knee joint. Compared with the model group, the expression of COLA2, GPX4, and SLC11 proteins in the articular cartilage of the OK group significantly increased (P<0.1), while the expression of MMP13 (P<0.1), AGEs (P<0.01), and receptor RAGE (P<0.01) decreased. The serum levels of TNF-α, VEGF, IL-6, MDA, and ROS in the OK group were significantly reduced (P<0.01), while SOD and GSH increased (P<0.01). In cell experiments, the levels of MDA (P<0.05), IL-6, and Fe2+increased in the IL-1 β group (P<0.01), while the levels of GSH (P<0.05) and SOD decreased (P<0.01); The protein levels of MMP13 increased (P<0.05), while the protein levels of COLA2, GPX4, and SLC11 decreased (P<0.01). OK intervention reverses the above results, improves oxidative stress and chondrocyte metabolic balance, reduces inflammatory factors, iron load, and ferroptosis. AGEs weakened the effect of OK, and the relevant indicators had statistical significance. In addition, OK further enhances the anti-inflammatory and antioxidant stress effects of ferroptosis inhibitor Fer-1 on C28/I2 cells, and improves metabolic balance. Conclusion OK can inhibit ferroptosis and protect articular cartilage through the AGEs-RAGE axis, thereby exerting anti arthritis effects.
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A Comparative Study on the Protective Effects of Mongolian Medicines Danggong-3, Zandan-3 and Zadi-5 on Myocardial Ischemia-Reperfusion Injury in Mice

ZHANG Xiao-ru, JIN Rong, ZHOU Shu-hong, ZHANG Zhong-yue, SONG Xiao-xia, GAO Qian, GUO Na, DU Yul-u, YU Ling-ze, WANG Min-jie

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Objective To investigate the protective effects of three classic Mongolian medicines, Danggong-3 (DG-3), Zandan-3 (ZD-3), and Zadi-5 (ZD-5), on myocardial ischemia-reperfusion injury (MIRI) in mice, and to compare the efficacy of these three Mongolian medicines on MIRI. Methods Using 7-week-old male C57BL/6 mice, they were randomly divided into 6 groups: sham operation (Sham) group, model (Model) group, positive control group of Compound Danshen Dropping Pills (CDDP), Danggong-3 (DG-3) group, Zandan-3 (ZD-3) group, and Zadi-5 (ZD-5) group. The mice were administered drugs by gavage 14 days before the modeling. The reversible left anterior descending coronary artery ligation (LAD) method was used to establish the model, and the electrocardiogram ST segment of the mice was continuously monitored. The mice were sacrificed 24 hours or 7 days after reperfusion. The MIRI modeling and recovery status were determined by monitoring the ST segment of the electrocardiogram; TTC staining was used to observe the myocardial infarction area; hematoxylin-eosin (HE) staining and Masson staining were used to observe the pathological inflammatory changes in the ischemic area of the mouse heart; TUNEL cell apoptosis staining was used to determine the apoptosis of tissue cells; enzyme-linked immunosorbent assay (ELISA) was used to detect the level of mouse creatine kinase isoenzyme (CK-MB) in the serum; the activity detection kit was used to detect the lactate dehydrogenase (LDH), superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in the serum; in vitro cell experiments, the effects of three Tibetan medicines on the cell viability of human myocardial cells (AC16) after oxygen-glucose deprivation/reperfusion (OGD/R) treatment were compared by cell proliferation and cytotoxicity (CCK-8). Results Electrocardiogram (ECG) examination revealed that the average heart rate during reperfusion was higher than that during ischemia, indicating myocardial ischemia-reperfusion injury. Compared with the model group, the TTC staining results of the ZD-3, DG-3, and ZD-5 groups showed that the myocardial infarction area in mice was reduced (P < 0.05); HE and Masson staining results indicated that after administration of Tibetan medicine, the recruitment of inflammatory cells was reduced to varying degrees and the production of myocardial tissue fibrosis was inhibited (P < 0.05); in the TUNEL apoptosis detection, the apoptosis in the ZD-3 group was significantly reduced (P < 0.001); the CK-MB level in the serum of the ZD-3 group was significantly lower (P < 0.01); in addition, the detection of myocardial enzymes and oxidative stress indicators LDH, SOD, and MDA 24 hours and 7 days after MIRI showed that before and after modeling, administration of ZD-3, DG-3, and ZD-5 could reduce the LDH activity of myocardial enzymes, and the ZD-3 and DG-3 groups could reduce the production of oxidative stress factors (P < 0.01); finally, the in vitro experiment detected cell activity, and the ZD-3 group could increase the cell survival rate of AC16 cells after OGD/R (P < 0.05). Conclusions The Mongolian medicines DG-3, ZD-3 and ZD-5 all have protective effects on MIRI in mice. Among them, ZD-3 has a better protective effect on the heart. The mechanism is closely related to reducing the infiltration of inflammatory cells and inhibiting the formation of cardiac tissue fibrosis. Under these experimental conditions, it is preliminarily believed that Zandan-3 is a therapeutic heart medicine that can effectively inhibit MIRI.
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Preliminary establishment of the whole process supervision system for laboratory animal

HOU Jinlong, MENG Yujie, XU Tianqi, WANG Lan, WANG Xin, LI Wei, WANG Guoqing

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To strengthen the supervision of laboratory animal welfare and ethics, and ensure the animal welfare, a scientific regulatory system for the entire process was established. The system included 12 regulatory indexes. Targeted evaluation criteria were formulated based on the characteristics of the indexes. The methods of inspecting the sites and using specialized equipments such as small animal Micro CT and MRI were applied to supervise regulatory indexes. The system established a dynamic regulatory linkage mechanism that combines project approval review, process supervision, and final review. And the system implemented a regulatory process that combines online and offline methods. The system prevented the occurrence of incidents that violate technological ethics, standardized regulatory procedures, and provided reference for the supervision of welfare and ethics in the production and use of laboratory animal.
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Impacts of geniposide on proliferation, apoptosis, and autophagy of lung cancer cells by regulating AMPK/mTOR/ULK1 pathway

chendan, sunping

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Objective: To discuss the impacts of geniposide on proliferation, apoptosis, and autophagy of lung cancer cells by regulating adenosine monophosphate activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/unc-51 like kinase 1 (ULK1) pathway. Methods: A549 cells were divided into lung cancer group, low-dose geniposide group, medium-dose geniposide group, high-dose geniposide group, AMPK activator (MK8722) group, and high-dose geniposide+AMPK inhibitor (Compound C) group. 5-ethynyl-2"deoxyuridine (EdU) staining and CCK-8 method were used to detect cell proliferation. Flow cytometry was used to detect cell apoptosis. Transmission electron microscopy was used to observe the number of autophagosomes in A549 cells. QRT-PCR was used to detect the mRNA expression of proliferating cell nuclear antigen (PCNA), p53, p62, and Bcl-2 homologous domain protein (Beclin1) in A549 cells. Western blot was used to detect microtubule associated protein 1 light chain 3 (LC3), p-AMPK, p-mTOR, and p-ULK1 proteins in A549 cells. Results: For the lung cancer group, the low, medium, and high dose geniposide groups showed a decrease in EdU positive rate, OD450 value, PCNA and p62 mRNAs, and p-mTOR protein in A549 cells, and an increase in apoptosis rate, autophagosome number, p53 and Beclin1 mRNAs, and LC3-II/LC3-I, p-AMPK, and p-ULK1 proteins, the high-dose geniposide group showed the most prominent trend (P<0.05). For the lung cancer group, the MK8722 group showed a decrease in EdU positive rate, OD450 value, PCNA and p62 mRNAs, and p-mTOR protein in A549 cells, and an increase in apoptosis rate, autophagosome number, p53 and Beclin1 mRNAs, and LC3-II/LC3-I, p-AMPK, and p-ULK1 proteins (P<0.05). For the high-dose geniposide group, the high-dose geniposide+Compound C group showed an increase in EdU positive rate, OD450 value, PCNA and p62 mRNAs, and p-mTOR protein in A549 cells, and a decrease in apoptosis rate, autophagosome number, p53 and Beclin1 mRNAs, and LC3-II/LC3-I, p-AMPK, and p-ULK1 proteins (P<0.05). Conclusion: Geniposide may inhibit A549 cell proliferation, promote autophagy and apoptosis by activating AMPK/mTOR/ULK1 pathway.
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Research progress on key regulatory factors in the development and progression of pediatric neuroblastoma

Chen Huihui, Bian Jiaxin, Cai Jiabin, Ding Zheyu, Xiao Rui, Gu Weizhong, Taoting, Wang Jinhu

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Neuroblastoma (NB) is the most common extracranial solid tumor in children, characterized by high mortality and poor prognosis. With advances in molecular biology and genomics research, it has become increasingly clear that NB initiation and progression are driven by the dysregulation of complex molecular networks. To develop safer and more efficient precision diagnostic and therapeutic strategies, it is particularly important to gain a deeper understanding of the molecular mechanisms underlying NB pathogenesis. To deepen the understanding of NB, this article systematically reviewed key regulatory factors and their research progress from three dimensions: tumor development process (including abnormal proliferation, migration, invasion, and EMT), inflammatory response, and cell apoptosis. We exhibited the regulatory mechanisms of genes including MYCN, ALK, BDNF, and PHOX2B on the malignant biological behaviors of NB cells, analyzed the tumor-promoting effects of inflammatory signals including NF-κB, COX-2/PGE2, MyD88, and HMGB1, and illustrated the mechanisms of apoptosis-related factors including the Bcl-2 family, p53-MDM2 axis, and TRAIL. These findings not only deepen our understanding of the molecular pathological mechanisms of NB, but more importantly, reveal multiple therapeutic targets with translational potential, providing systematic theoretical references for basic research and clinical treatment of NB. Moreover, they also promote the research process from molecular mechanisms to clinical translation, ultimately aiming to improve the prognosis of pediatric patients.
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Research progress of neuropeptides in methamphetamine use disorder

ZHANG XIN JIE, HOU ZHEN PING, YANG GENG MENG, HOU YU HAN, XU JING, LI LI HUA, HONG SHI JUN

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Methamphetamine use disorder (MUD) is a refractory disorder worldwide with limited treatment options. Studies have found that neuropeptides may be a new target for the treatment of MUD. Studying the regulatory mechanism of neuropeptides on MUD may provide new options for the treatment of MUD. However, there are many kinds of neuropeptides, the mechanism of action is complex, and the clinical drug reference is limited. This review focuses on orexin (OX), oxytocin (OT), vasopressin (VP), neurotensin (NT), neuropeptide S (NPS), neuropeptide Y (NPY), somatostatin (SST), pituitary adenylate cyclase-activating peptide (PACAP), vasoactive intestinal peptide (VIP), glucagon-like peptide-1 (GLP-1) and so on The regulatory role and mechanism of the peptide in MUD. This article provides new ideas for the treatment of MUD and promotes its application in the treatment of MUD.
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The impacts of miR-101-3p on VEGFA/PI3K/AKT pathway, inflammatory response, and pregnancy outcome in rats with hypertensive disorder of pregnancy

xiemaohua

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Objective: To investigate the impacts of microRNA-101-3p (miR-101-3p) on the vascular endothelial growth factor A (VEGFA)/phosphatidylinositol 3-kinase (PI3K)/serine threonine protein kinase (AKT) pathway, inflammatory response, and pregnancy outcomes in rats with hypertensive disorder of pregnancy (HDP). Methods: The expression of miR-101-3p and VEGFA in serum samples of 60 normal pregnant women (control group) and 60 HDP pregnant women (HDP group) who underwent regular prenatal check-up in our hospital from March 2024 to October 2024 were detected by qRT-PCR. The HDP rat model was constructed, and successfully modeled rats were stochastically divided into HDP group, NC antagomir group (tail vein injection of NC antagomir), and miR-101-3p antagomir group (tail vein injection of miR-101-3p antagomir). Another 10 normal pregnant rats were used as the Control group, and equal amounts of physiological saline were injected into both the Control group and the HDP group. The blood pressure, 24-hour urine protein, and pregnancy outcomes of rats in each group were measured. QRT-PCR was used to detect the expression of miR-101-3p in placental tissue of HDP rats. ELISA kit was used to detect the expression of inflammatory factors and vascular injury factors in serum. Western blot was used to detect the expression of VEGFA, PI3K, and AKT proteins in placental tissue. Results: The expression of miR-101-3p was high and VEGFA was low in HDP group (P<0.05).The morphology and structure of placental tissue in the Control group were normal; the placental tissue structure of the HDP group and NC antagomir group was blurred, with a large amount of inflammatory cell infiltration visible; the placental tissue damage and inflammatory cell infiltration of pregnant mice in the miR-101-3p antagomir group were reduced. The blood pressure, 24-hour urinary protein, miR-101-3p, IL-1β, IL-6, TNF-α, sICAM-1, and ET-1 in the HDP group were higher than those in the control group, while the embryo survival rate, NO, VEGFA mRNA and protein, PI3K, and AKT were lower than those in the control group (P<0.05). The blood pressure, 24-hour urinary protein, miR-101-3p, IL-1β, IL-6, TNF-α, sICAM-1, and ET-1 in the miR-101-3p antagomir group were lower than those in the HDP group and NC antagomir group, while the embryo survival rate, NO, VEGFA mRNA and protein, PI3K, and AKT were higher than those in the HDP group and NC antagomir group (P<0.05). Conclusion: Inhibiting miR-101-3p can activate the VEGFA/PI3K/AKT pathway, suppress inflammatory response and vascular damage, and ameliorate pregnancy outcomes.
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RIPC increases neuronal hypoxic-ischemic tolerance via plasma exosomes

ZHANG Zhiyong, WANG Xiaojie, SHAO Guo

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Objective To investigate whether remote ischemic preconditioning (RIPC) exerts a neuroprotective effect against hypoxic ischemia by decreasing neuronal DNA methyltransferases (DNMTs) levels via plasma exosomes. Methods C57BL6 mice were RIPC with simultaneous tail vein injection of the exosome inhibitor GW4869, and 1 hour later, middle cerebral artery occlusion (MCAO) was performed, and the mice were randomized into four groups. Bederson score and cornering test to assess the degree of neurologic impairment. Expression levels of DNA methyltransferases (DNMTs) and nerve damage-related genes in the mouse cerebral cortex using real time PCR and Western blot. Plasma exosomes were extracted from mice before and after RIPC, and co-cultured with mouse neuronal cells HT22 for Oxygen glucose deprivation (OGD). Detection of cell viability by CCK8. The cell morphology and the fluorescence intensity of the anti-apoptotic protein Bcl-2 were observed by immunofluorescence, and the mRNA and protein expression levels of DNMTs and related apoptotic genes (Caspase-3, BAX, and Bcl-2) were detected in the cells. Results The results of Bederson scores and cornering experiments showed that RIPC intervention significantly improved neurological deficits after MCAO in mice, and its neuroprotective effect was significantly attenuated after the administration of GW4869. RIPC treatment down-regulated the expression of DNMTs, Caspase-3 and BAX and up-regulated the expression of Bcl-2 in the cerebral cortex of MCAO mice. In vitro results showed that RIPC-derived exosomes reduced the expression of DNMTs, enhanced the fluorescence intensity of Bcl-2 and improved cell morphology in HT22 cells under OGD conditions, while down-regulating the expression of Caspase-3 and BAX and enhancing cell viability. Conclusion RIPC may play a neuroprotective role by downregulating the expression of DNMTs through plasma exosome-mediated manner and inhibiting the expression of Caspase3 and BAX, increasing the expression of Bcl-2, inhibiting neuronal apoptosis, and enhancing the tolerance of neuronal cells to the hypoxic-ischemic environment.
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Research on the Mechanism of "Three Methods and Three Points" Massage in Improving Motor Function of SNI Rats by Delaying Denervated muscle Atrophy

YANJIAWANG, Xu Yue, Yu Tianyuan, Naren Tuya, Zhang Yingqi, Zhang Hongzheng, Liu Jiayue, , Zhang Hanyu, Sun Jiawei

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【Abstract】 Objective：To explore the mechanism by which "three techniques and three acupoints" massage improves the motor function of SNI rats by delaying denervated muscle atrophy. Methods: Thirty-six male SD rats were randomly divided into normal group (n=9), sham operation group (n=9), model group (n=9), and massage group (n=9). The model group and massage group were subjected to SNI model establishment by clamping method; the sham operation group only exposed the sciatic nerve without clamping. From the 7th day after surgery, the massage group rats were intervened. An intelligent massage technique simulation instrument was used to apply point, pull, and knead techniques to Yinmen, Chengshan, and Yanglingquan acupoints in sequence. Each acupoint was treated with each technique for 1 minute, once a day. After 10 interventions, a 1-day rest was taken, followed by another 10-day intervention; the sham operation group and model group rats only received the same duration of grasping and fixation treatment; the normal group maintained routine feeding conditions. The hind limb grip force was measured before modeling, after 10 and 20 interventions to evaluate muscle strength. After 20 massage sessions, the rats were sacrificed and the right gastrocnemius muscle was taken for HE staining to observe the muscle atrophy and measure the cross-sectional area of muscle fibers; RT-PCR was used to detect the expression of CCNB1, CNTF, and MEF2A mRNA in the right gastrocnemius muscle tissue; Western-blot was used to detect the expression of PAX3, Desmin, HGF, and MEF2C proteins in the right gastrocnemius muscle tissue; immunofluorescence was used to detect the expression of MEF2C protein in the affected gastrocnemius muscle. Results： Compared with the normal group and sham operation group, the hind limb grip force of the model group rats was significantly reduced (P<0.01); the muscle fibers of the model group rats were disordered, the muscle cells were significantly atrophied, and the cross-sectional area was significantly reduced (P<0.01), and the expression of CCNB1, CNTF, MEF2A mRNA and PAX3, Desmin, HGF, and MEF2C proteins was lower than that of the normal group and sham operation group (P<0.05). Compared with the model group, the hind limb grip force of the massage group rats was significantly increased (P<0.01), the muscle fibers were atrophied but arranged orderly without obvious disorder, and the cross-sectional area was significantly increased (P<0.01), and the expression of CCNB1, CNTF, MEF2A mRNA and PAX3, Desmin, HGF, and MEF2C proteins was significantly upregulated (P<0.05). Conclusions "Three techniques and three acupoints" massage can promote the expression of CCNB1, CNTF, MEF2A mRNA and PAX3, Desmin, HGF, and MEF2C proteins, promote the proliferation and differentiation of muscle satellite cells and repair nerve injury, delay denervated muscle atrophy, and improve the motor function of SNI rats.
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The Role of the NLRP3 Signaling Pathway in MASLD and the Intervention of Traditional Chinese Medicine

Zhang Tianyu, Wang Yinghang, Panzhi

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Metabolic dysfunction-associated steatotic liver disease (MASLD) is a globally prevalent chronic liver disease. As a complex condition caused by multiple factors, the exact pathogenesis of MASLD remains incompletely understood. Studies have shown that inflammation plays a central role in the pathological development of MASLD. NOD-like receptor family pyrin domain containing 3 (NLRP3), as a critical immune regulatory factor, plays a pivotal role in the [1]inflammatory response of MASLD. Overactivation of NLRP3 exacerbates chronic liver inflammation and promotes fat accumulation in the liver. Furthermore, excessive activation of NLRP3 leads to the generation of reactive oxygen species (ROS), which further activates immune response cells, thereby intensifying liver damage. Consequently, inhibiting NLRP3 inflammasome activation has become one of the new strategies for treating MASLD. Numerous studies have indicated that extracts and formulations of Traditional Chinese Medicine (TCM) can effectively alleviate the inflammatory response in MASLD by inhibiting NLRP3 activation, achieving significant progress in the clinical treatment of MASLD. This article reviews the role of the NLRP3 signaling pathway in MASLD and the potential of TCM in improving MASLD by regulating NLRP3 inflammasome activity, providing a reference for the prevention and treatment of MASLD with TCM.
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Construction and Application Evaluation of a Rat Model of Liver Depression Based on Data Mining

wangning, DING YING, zheng na, huang zi meng, liu tong hua

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Objective: To explore the methods of establishing and evaluating the rat model of liver depression syndrome, and provide a reference for the standardized development of this model.Methods: Computer searches were conducted in databases such as CNKI, Wanfang, and VIP for experimental literature related to the rat model of liver depression syndrome from November 14, 2019, to November 14, 2024. The literature was screened according to the set inclusion and exclusion criteria. Information such as the publication time, animal conditions, related diseases, modeling methods, modeling time, evaluation indicators, and intervention methods in the literature was extracted. Software such as Excel 2021 and IBM SPSS Modeler 18.0 were used for data collation, frequency analysis, association rule analysis, and the results were visually displayed in the form of charts.Results: A total of 188 eligible literatures were finally included. The commonly used rats in the rat model of liver depression syndrome were Sprague-Dawley (SD) rats (75.53%), mostly male (62.77%), and most of them were specific pathogen-free (SPF) grade (82.45%). The related diseases were mainly digestive system diseases (59.39%). Among the syndrome types, the liver depression and spleen deficiency syndrome was the most common (62.96%). The multi-factor method was mostly used for the modeling method (55.03%), and the modeling time was concentrated within 18-21 days. At the same time, potential combinations of macroscopic syndrome evaluation indicators were obtained, and the intervention method was mainly Chinese medicine compound prescriptions (86.42%).Conclusion: The rat model of liver depression syndrome is widely used, but currently there are problems such as non-standard names of syndrome types, lack of unified standards for modeling methods, and imperfect evaluation systems. This study provides ideas and references for the standardization of syndrome types, model optimization, and improvement of the evaluation system of the rat model of liver depression.
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Research Progress on Podocyte Injury Caused by Mitochondrial Dysfunction in Diabetic Nephropathy

Ma Qianqian, Wang Jinjin

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Diabetic kidney disease (DKD) is a leading cause of end-stage renal disease, characterized by pathological changes such as decreased glomerular filtration rate and proteinuria. As a key component of the glomerular filtration barrier, podocyte injury is closely associated with the progression of DKD. Recent studies have revealed that mitochondrial dysfunction plays a central role in podocyte injury in DKD, primarily manifested as enhanced mitochondrial oxidative stress, defective autophagy, and fission/fusion imbalance. These alterations lead to excessive production of reactive oxygen species and inflammatory factors, thereby accelerating podocyte apoptosis. Meanwhile, multiple signaling pathways-including NOX4/TRPC6, TGF-β1/SMAD, AMPK/PGC-1α, and PINK1/Parkin-can intervene in mitochondrial damage-induced podocyte apoptosis, while dysregulation of genes related to podocyte mitochondrial function exacerbates DKD. This article systematically reviews the critical roles of relevant signaling pathways and mitochondrial DNA in mediating podocyte mitochondrial injury during DKD progression, aiming to provide new theoretical foundations and therapeutic targets for DKD prevention and treatment. Additionally, it explores the potential of traditional Chinese medicine targeting podocyte mitochondria as a strategy to delay DKD progression.
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Mechanism of ID-1 promoting MCF-7 cell progression in human breast cancer by activating NF-κB/SHP2/SMAD/Src signaling pathway

wuxueliang, Zhou Haifeng

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Objective: To explore the expression and clinical significance of ID-1 in breast cancer and the molecular mechanism of regulating the progression of human breast cancer MCF-7 cells by targeting NF-κB/SHP2/SMAD/Src signaling pathway; Methods: Immunohistochemistry was used to detect the expression of ID-1 in breast cancer tissues and adjacent normal tissues, and its clinical significance was analyzed. The correlation between ID-1 and key proteins was analyzed by bioinformatics. In an in vivo experiment, 45 female mice were used to establish a breast cancer model and were divided into 5 groups: NC group (Group 1), BMP2 group (Group 2), ID-1 mimic+BMP2 group (Group 3), BMP2+PHPS1 group (Group 4), and ID-1 mimic+PHPS1 group (Group 5). Tumor tissues from the five groups of mice were dissected, observed, and weighed. In an in vitro experiment, Human breast cancer MCF-7 cells were divided into 7 groups: NC group (Group 1), BMP2 group (Group 2), ID-1 mimic+BMP2 group (Group 3), sulfasalazine+BMP2 group (Group 4), ID-1 mimic+sulfasalazine+BMP2 group (Group 5), BMP2+PHPS1 group (Group 6), and ID-1 mimic+BMP2+PHPS1 group (Group 7). Western blot analysis was conducted to assess protein expression in the various groups. Scratch assays were used to evaluate MCF-7 cell migration, while Transwell assays were employed to assess MCF-7 cell invasion; Results: Immunohistochemical results showed that the expression of ID-1 in breast cancer tissues was significantly higher than that in adjacent normal tissues, mainly in the nucleus and cytoplasm, and the difference was statistically significant (P<0.001). The expression status of ID-1 was closely related to histological grade, TNM stage, lymph node metastasis and distant metastasis, and the differences were statistically significant, P<0.05; Bioinformatics correlation analysis indicated that ID-1 was correlated with BMP2, NF-κB, SHP2, SMAD and Src in breast cancer. The results of in vivo experiments showed that ID-1 was proved to promote the progression of breast cancer tumors, while inhibition of SHP2 slowed down tumor progression. The results of in vitro experiments showed that inhibition of SHP2 led to significant decreases in the expression of ID-1, NFκB, P-SHP2, P-SMAD1/5/8, and P-Src proteins. Similarly, inhibition of NF-κB resulted in reduced expression of ID-1, NF-κB, P-SHP2, P-SMAD1/5/8, and P-Src proteins. Scratch assays demonstrated that both ID-1 and BMP2 promoted MCF-7 cell migration, while inhibition of SHP2 or NF-κB significantly reduced cell migration. Transwell assays revealed that ID-1 and BMP2 enhanced MCF-7 cell invasion, with inhibition of SHP2 or NFκB leading to a marked reduction in cell invasion. Conclusion: ID-1 may promote breast cancer invasion and migration by activating the NFκB/SHP2/SMAD/Src signaling pathway.
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Research Progress of Traditional Chinese Medicine in the treatment of Rheumatoid Arthritis by regulating Wnt/β-catenin signaling pathway

taozhijuan, yangbeijun, chengshaomin, zhangjinlian, zhangzhang

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Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic synovitis and pannus formation, with an unknown etiology. The Wnt/β-catenin signaling pathway has emerged as a critical therapeutic target for RA. In recent years, significant progress has been made in related research; however, systematic reviews and integrated analyses remain inadequate. Based on this context, this article explores the mechanisms underlying the role of the Wnt/β-catenin signaling pathway in the pathological progression of RA, including its regulation of inflammatory responses, fibroblast-like synoviocyte (FLS) proliferation, apoptosis, bone destruction, and angiogenesis pathways. Furthermore, it summarizes the latest research advancements in the modulation of the Wnt/β-catenin signaling pathway by traditional Chinese medicine (TCM) monomers (such as phenolics, terpenoids, and quinones) and TCM compound formulations (including Chinese patent medicines and other compound types) for the treatment of RA. The aim is to provide theoretical foundations and reference directions for clinical applications and the development of novel drugs for RA.
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Research Advances on Epigenetic Technologies for Mechanistic and Therapeutic Research in sepsis induced myocardial injury

WANG Xiaoxuan, XIAO Lu

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Sepsis-induced myocardial injury (SIMI) is a common and critically fatal complication of sepsis. Its pathogenesis has not been fully elucidated, involving multiple pathological processes such as excessive inflammatory response, mitochondrial dysfunction, apoptosis, and oxidative stress. Although current clinical interventions primarily include fluid resuscitation, vasoactive agents, and anti-inflammatory therapies, their efficacy remains limited and fails to reverse pathological remodeling at the epigenetic level. This article systematically summarizes and discusses studies on epigenetic modifications—including DNA methylation, histone modifications (e.g., acetylation, methylation), and non-coding RNA (ncRNA) regulation—in relation to septic myocardial injury. The review aims to provide novel perspectives for early warning, diagnosis, treatment, and targeted drug development for SIMI, thereby improving the prognosis of patients with sepsis-induced myocardial injury.
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Therapeutic strategy of traditional Chinese medicine for endometriosis based on Wnt/β-catenin signaling pathway study

leikaikai, guojinnan, xiangrong, lixiaolong, fengxiaoling, xufang, kuanghongying, maoxin, sunmiao

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Endometriosis (EMs) is a common estrogen-dependent disease in women of childbearing age, which often leads to chronic pelvic pain, infertility, ovarian cancer and other serious complications, jeopardizing the health of women.The pathogenesis of EMs is complex and involves the alteration of multiple signaling pathways mediated by hormones, immunity, genetics and environment and their interactions.Wnt/β-catenin signaling is involved in the regulation of embryonic development and tissue homeostasis, and recent studies have revealed that it may be involved in the pathogenesis of EMs in multiple ways. The Wnt/β-catenin signaling pathway is involved in the regulation of embryonic development and tissue homeostasis, and has been found to be involved in the pathogenesis of EMs through multiple pathways in recent years. Based on this, this paper systematically describes the biological characteristics of the Wnt/β-catenin signaling pathway, summarizes the main mechanisms and signaling pathways involved in the pathogenesis of EMs, as well as the current status of research on the regulation of this signaling pathway by traditional Chinese medicine for the intervention of EMs. We aim to clarify how the Wnt/β-catenin signaling pathway affects the development of EMs, and in the future, we should focus on exploring whether it can become one of the indicators for clinical prediction and early diagnosis of EMs, so as to provide theoretical support for the early diagnosis of EMs and the research and development of targeted drugs.
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miR-574-5p improves cardiac function in mice after cardiac arrest by targeting TNS1Wang Qiuyan1^{, Wang Xiaolei}1^{, Yu Meijun}1^{, Chen Jing}2^{, Lou Xusheng}3^*

wangqiuyan, wangxiaolei, yumeijun, chenjing, louxusheng

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Objective This study focused on the regulatory relationship between TNS1 and miR-574-5p in cardiac arrest and its clinical significance, and verified the therapeutic potential of targeted inhibition of miR-574-5p. Methods Oxygen-glucose deprivation/reoxygenation (OGD/R) cardiomyocyte models and mouse cardiac arrest/cardiopulmonary resuscitation (ACA/CPR) models were established. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression levels of miR-574-5p and TNS1; the targeting relationship between miR-574-5p and TNS1 was verified by dual-luciferase reporter gene assay; cell viability was detected by CCK-8 assay; apoptosis was measured by flow cytometry; the levels of cardiac injury marker cTnI and oxidative stress markers MDA and 4-HNE in serum were detected by enzyme-linked immunosorbent assay (ELISA); the hemodynamic monitoring system was used to evaluate the cardiac function indices dp/dtmin and dp/dtmax; echocardiography was performed to determine cardiac function parameters such as left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS). Results OGD/R treatment significantly upregulated the expression of miR-574-5p and inhibited the expression of TNS1 in cardiomyocytes. Inhibition of miR-574-5p improved the survival rate of cardiomyocytes and alleviated oxidative stress injury. In the ACA/CPR model, the miR-574-5p antagonist group significantly improved cardiac function indices, reduced the levels of cardiac injury and oxidative stress markers, and reversed the upregulated miR-574-5p and downregulated TNS1 expression patterns in myocardial tissues. Conclusion This study confirmed that targeted inhibition of miR-574-5p can improve cardiac function by upregulating the expression of TNS1, providing a new therapeutic target for myocardial protection after cardiac arrest.
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Analysis on Journal Impact Evaluation and High Quality Development Based on CNKI——Taking Acta Laboratorium Animalis Scientia Sinica and Chinese Journal of Comparative Medicine as Examples

shenyuanyuan

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Objective To analyze the influence of Acta Laboratorium Animalis Scientia Sinica and Chinese Journal of Comparative Medicine through CNKI big data, objectively analyze and evaluate the data, display the current development status of the journals, and propose high-quality development suggestions. Method CNKI was used as the statistical data source, and relevant quantitative data from the "Annual Report on the Impact Factors of Chinese Academic Journals" were used. Bibliometric methods were employed to quantitatively analyze the publication characteristics indicators of the two journals from 2021 to 2023, including citation count, number of funded papers, publication delay, composite total citation frequency, and composite impact factors. Result During the statistical period of 2021-2023, the publication scale of the two journals was moderate, the number of funded papers was relatively high, the publication delay was relatively long, and there was significant room for improvement in the composite total citation frequency and composite impact factor. Conclusion The high-quality development of academic journals should focus on content construction, strengthen scientific research cooperation, do a good job in brand promotion, apply advanced technology, carry out professional writing guidance and training, and regularly conduct academic influence evaluations.
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The exploration of the non-human primate anatomical operation risk assessment and control measures in the high-level biosafety laboratory

ZHENG Xiaoqi, XUE Senren, ZHANG Xianyu, YANG Jiaxin, CHEN Yuyu, LI Xiaobo, LIN Jingwen, ZHANG Yabin, HAN Jianbao

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Non-human primate (NHP) animal models are the core tools for the study of highly pathogenic pathogenic microorganisms, and are irreplaceable in the fields of pathological mechanism and drug discovery. However, the risk of anatomical sampling of NHP infection models in high-level biosafety laboratories is prominent, and there is a lack of research on related risk assessment and control measures. Based on biosafety regulations and practical experience, this paper systematically discusses the risk control strategies of anatomical operations from the dimensions of personal protection, instrument selection, anatomical specifications, documentation system and personnel training, aiming to improve the biosafety management level of high-level laboratories, reduce the risk of pathogen leakage and human infection, and provide safety support for the research of highly pathogenic pathogenic microorganisms.
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Reserpine-Induced Depressive Behaviors and Neural Impairment in Rats: Role of BDNF/AKT1 Signaling Suppression

ZHOU Guili, HE Junhui, YANG Li, ZHOU Rongfei, WEI Guining, LAI Kedao, LI Li, HUANG Renbin

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Objective This study aims to systematically elucidate the molecular mechanism of reserpine-induced depression through network toxicology, molecular docking techniques, behavioral assessments of animal models, and histopathological analyses. Methods Core targets were screened using multi-database network toxicology, followed by constructing a protein-protein interaction (PPI) network and validating core targets through molecular docking. Sprague-Dawley (SD) rats were randomly divided into a control group and a reserpine-treated group (0.5 mg·kg?1), receiving corresponding treatments once daily for 4 consecutive days. Behavioral changes were assessed using the forced swim test and open field test. Serum neurotransmitters were quantified by enzyme-linked immunosorbent assay (ELISA). Neuropathological damage was observed via tissue staining. Target gene expression regulation was verified through Western blotting. Results Network toxicology screening and molecular docking simulation results demonstrated that reserpine exhibited significant binding affinity with dopamine D2 receptor (DRD2), cyclic-AMP response element binding protein (CREB), and serine/threonine-protein kinase 1 (AKT1). Animal experiments demonstrated that the treated group displayed depression-like behaviors including motor inhibition (P<0.05), with decreased serum levels of norepinephrine (NE) and 5-hydroxytryptamine (5-HT) (P<0.05，P<0.05). Pathological observations revealed microglial proliferation in the cerebral cortex, increased apoptosis, and reduced Nissl bodies in the hippocampal CA1 region. Downregulation of brain-derived neurotrophic factor (BDNF) in brain tissue, along with decreased expression of hippocampal AKT1 and phosphorylated AKT1 (p-AKT1), was also observed. Conclusion Reserpine has been demonstrated to exert an influence on monoamine transmitter metabolism and neuronal structural integrity through the inhibition of BDNF and AKT1 protein expression, which can result in the manifestation of depressive-like behavior and cerebral nerve damage in rats.
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Study on the Improvement of Skin Lesions and Anti inflammatory Effects of Qingxin Yunpi Formula in Mice with Food Allergic Atopic Dermatitis

Yin Yi, Zhai Panpan

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Objective: To investigate the therapeutic effect of Qingxin Yunpi Formula on food allergy (FA) - related atopic dermatitis (AD) model mice induced by 2,4-dinitrochlorobenzene (DNCB)+ovalbumin (OVA). Method: BALB/c male mice were randomly divided into blank group, AD group, ADFA model group, Qingxin Yunpi Formula medium dose group, Qingxin Yunpi Formula high-dose group, and prednisone group, with 10 mice in each group. Except for the blank group and AD group, all other groups were treated with DNCB on the back and OVA was injected intraperitoneally to establish an ADFA model. The AD group was treated with DNCB on the back. At the end of modeling, the condition of skin lesions, dermatitis scores, and scratching behavior were recorded. Skin pathology, epidermal thickness, and mast cell infiltration were observed. Enzyme linked immunosorbent assay (ELISA) was used to detect serum OVA specific IgE (OVA sIgE) levels and serum cytokine levels of interleukin-4 (IL), IL-5, and interferon (IFN) - γ. Immunohistochemistry (HIC) was used to detect the expression of IL-4, IL-5, and IFN - γ proteins in the skin lesion tissue. Result: Compared with the blank group and AD group mice, the ADFA model group mice had severe back skin lesions, increased dermatitis score and scratching frequency, thickened back epidermis and spinous layer, and more inflammatory cell infiltration in the dermis layer. The serum OVA sIgE level of mice increased, and the serum cytokine IL-4, IL-5, IFN - γ levels increased. The expression of IL-4, IL-5, IFN - γ protein in the skin lesion tissue also increased; Compared with the ADFA model group, the mice in each treatment group showed improvement in back skin lesions, dermatitis scores
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Effect of mitochondrial function mediated by PLD1 on lung of bronchopulmonary dysplasia model mice

Jin Lü

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objective: To investigate the effect of mitochondrial function mediated by phospholipase D1(PLD1) on lung of mice with bronchopulmonary dysplasia (BPD). Methods: Eighteen WT mice and 18 PLD1-KO mice were divided into the following four groups: normoxic +WT group, normoxic +PLD1-KO group, hyperoxic +WT group and hyperoxic +PLD1-KO group, with 9 mice in each group. The newborn mice in hyperoxia group were exposed to hyperoxia (85%O2) for 14 days. In normoxic group, newborn mice were exposed to normoxic conditions (21%O2) for 14 days. On the 14th day, the levels of oxidative stress, apoptosis and fibrosis in mice lungs were evaluated by commercial kits [malondialdehyde (MDA) and superoxide dismutase (SOD)], protein blot (Bax, Bcl-2, cleaved caspase-3) and immunohistochemistry (α-SMA, AIF). MLE-12 cells were divided into normoxic +si-NC, hyperoxic +si-NC, normoxic +si-PLD1 and hyperoxic +si-PLD1. After transient transfection, the cells were exposed to normoxia or hyperoxia for 24 h. Mitochondrial reactive oxygen species (ROS) and function were measured by MitoSOX Red and hippocampus mitochondrial stress test. Results: Compared with the normoxic group, α-SMA, AIF positive staining, MDA, Cleaved Caspase-3 and BAX in lung tissue of hyperoxic group increased significantly (P < 0.05), while SOD activity and BCL-2 decreased significantly (P < 0.05). The positive staining of α-SMA, AIF, the abundance of Cleaved Caspase-3 and BAX in lung tissue of hyperoxia +PLD1-KO group were lower than those of hyperoxia +WT group (P < 0.05), while the SOD activity and BCL-2 abundance were higher than those of hyperoxia+WT group (P < 0.05). Compared with normoxic group, the expression of AIF in mitochondria of MLE-12 cells in hyperoxic group decreased significantly (P < 0.05), but it increased significantly in cytoplasm (P < 0.05), and compared with hyperoxic +si-NC group, the expression of AIF in mitochondria of MLE-12 cells in hyperoxic +si-PLD1 group increased significantly (P < 0.05). The abundance of mtROS in MLE-12 cells in hyperoxia group was higher than that in normoxia group (P < 0.05), and the abundance of mtROS in MLE-12 cells in hyperoxia +si-PLD1 group was lower than that in hyperoxia +si-NC group (P < 0.05). Compared with normoxic +si-NC group, the basic respiration, ATP production, maximum respiration and standby respiration of hyperoxic +si-NC group decreased significantly (P < 0.05). Compared with hyperoxia +si-NC group, hyperoxia +si-PLD1 group significantly increased the basic respiration, ATP production, maximum respiration and standby respiration (P < 0.05). Conclusion: The key role of PLD1 in hyperoxia-induced mouse BPD and MLE-12 cells, the deletion of PLD1 gene may protect lung injury induced by hyperoxia exposure by resisting mitochondrial apoptosis.
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Comparative Study on the Pharmacological Activities of Angelica Sinensis and Its Fractions in Tonifying Blood and Moistening Intestines

SHI Yucun, HOU Xuemei, DONG Xiaoli, YANG Qianqian, MENG Ziying, WU Guotai

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Objective: To compare the differences in the hematinic and laxative pharmacological activities of Angelica sinensis and its components. Methods: Eighty-four Kunming mice were randomly divided into a normal group, a model group, a positive control group, a whole Angelica sinensis group (AS group), an Angelica sinensis water-soluble component group (AW group), an Angelica sinensis alcohol-soluble component group (AE group), and an Angelica sinensis volatile oil group (AO group), totaling eight groups, with 12 mice in each group. Except for the normal group, the remaining groups were subcutaneously injected with N-Acetylphenylhydrazine (APH) and orally administered with loperamide hydrochloride to establish a mouse model of blood deficiency constipation. On day 7 of modeling, each group was orally administered the corresponding test substance once daily for three consecutive days. General conditions and body weight changes of the mice were observed, peripheral blood cell counts were measured, stool morphology and fecal output were recorded, fecal moisture content and colonic tissue moisture content were detected, small intestine propulsion rate was assessed by charcoal meal method, and serum levels of β-endorphin (β-EP), cholecystokinin octapeptide (CCK-8), substance P (SP), and vasoactive intestinal peptide (VIP) were determined by ELISA. Differences in the hematinic and laxative pharmacological activities of Angelica sinensis and its components were analyzed. Results: Compared with the normal group, the model group mice showed significantly reduced white blood cells (WBC), red blood cells (RBC), hemoglobin (HGB), hematocrit (HCT), platelet count (PLT), and body weight (P<0.05 or P<0.01). Additionally, fecal moisture content, colon moisture content, and small intestine propulsion rate were decreased (P<0.05 or P<0.01). Serum CCK-8 and SP levels were also lower (P<0.01), while serum β-EP and VIP levels increased (P<0.05). Compared with the model group, AS and AW groups had higher RBC, WBC, HGB, PLT, HCT, defecation volume, fecal moisture content, and colon moisture content (P<0.05 or P<0.01). The AE group showed increased RBC, WBC, HGB, PLT, HCT, and colon moisture content (P<0.05 or P<0.01), but had a lesser effect on defecation volume and fecal moisture content. The AO group exhibited increased fecal moisture content, colon moisture content, and defecation volume (P<0.05 or P<0.01), but no significant changes in RBC, WBC, HGB, PLT, and HCT. The AE group showed no significant changes in defecation volume, fecal moisture content, and colon moisture content. The AS and AO groups had increased small intestine propulsion rates (P<0.01), while there was no significant difference in small intestine propulsion rate between the AW and AE groups. The AS group had elevated serum CCK-8 and SP levels (P<0.01) and decreased serum β-EP and VIP levels (P<0.01). The AO group had increased serum CCK-8 and SP levels (P<0.05), but no significant change in serum β-EP and VIP levels. The AW group had decreased serum VIP levels (P<0.05), but no statistically significant difference in serum CCK-8 and SP levels. Compared with the AS group, the AW group had higher RBC, WBC, HGB, PLT, and HCT levels, while the AO and AE groups had lower levels of these parameters (P<0.05). Both AW and AO groups had increased fecal moisture content (P<0.05), and both AW and AE groups had increased colon moisture content (P<0.05). All three groups (AO, AE, and AW) had elevated serum CCK-8 and SP levels and decreased serum β-EP and VIP levels (P<0.05). In summary, AE > AW > AS > AO in terms of blood replenishment, AO > AS > AW > AE in terms of promoting bowel movements, and AO > AS > AE > AW in terms of intestinal motility. Conclusion: Angelica sinensis and its components have varying degrees of blood replenishing and bowel-promoting activities. The AE component has strong blood replenishing activity, while the AO component has strong bowel-promoting and defecation-stimulating activity, providing a reference for the development of traditional Chinese medicine based on Angelica sinensis components.
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Progress in research on TREM macrophage mediated signaling pathways in myocardial infarction

Wang Jing, Wang He, Wang Xia, Li Shi-long, Zhao Zhuo

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Myocardial infarction (MI) is a critical and highly fatal cardiovascular disease that seriously threatens patients "lives. More possible new targets need to be explored to protect heart function and prevent the progression of heart failure. The Triggering Receptor Expressed Myeloid Cell (TREM) is an activating transmembrane receptor belonging to the immunoglobulin superfamily. TREM-1 and TREM-2 are the most important family members, and are mostly expressed on the surface of myeloid cells. The two have similar transmembrane glycostructural proteins, but they play different roles in regulating inflammatory responses. Myeloid cell-triggered receptors play an important role in the inflammatory response, myocardial remodeling, and myocardial cell regeneration after myocardial infarction. This article introduces the biological functions, expression forms, and ligand combinations of TREM-1 and TREM-2, and discusses the role of their mediated signaling pathways in myocardial infarction to find potential new targets for the treatment of myocardial infarction diseases.
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Mechanism Study of Yiqi Huoxue Lishui Formula on Mitochondrial Energy Metabolism Regulation in Heart Failure Rats Based on the AMPK/PGC-1α Signaling Pathway

ZHUANG Rui1, xuedonghua, LI Le, MA Liyong, GAO Qun, ZHANG Lijing, PAN Yi

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Objective To investigate the effects of Yiqi Huoxue Lishui Formula (YQHXLSF) on mitochondrial morphology and function in heart failure (HF) rats by activating the AMPK/PGC-1α signaling pathway. Methods HF models were established by left anterior descending coronary artery (LAD) ligation combined with starvation and exhaustive swimming. Postoperatively, rats were randomly divided into sham, model, trimetazidine (TMZ), YQHXLSF medium-dose (M), and high-dose (H) groups. After 4 weeks of treatment, cardiac function was assessed using echocardiography and HE/Masson staining. ROS levels, mitochondrial ultrastructure, and functional changes were detected. Protein expression of the AMPK/PGC-1α pathway was measured by Western blot, while mRNA expression and mitochondrial DNA (mtDNA) replication levels were evaluated using Real-time PCR. Results YQHXLSF significantly improved cardiac function indices, attenuated myocardial fibrosis, reduced ROS levels, enhanced mitochondrial respiratory chain complex activity and membrane potential, and increased ATP content. Western blot and Real-time PCR results demonstrated that YQHXLSF upregulated the expression of p-AMPK, PGC-1α, NRF-1, and TFAM at both protein and mRNA levels, and promoted mtDNA replication. Conclusion YQHXLSF improves cardiac function and myocardial fibrosis, reduces ROS levels, maintains mitochondrial structural and functional stability, promotes mitochondrial biogenesis, and regulates mitochondrial energy metabolism to increase ATP production in HF rats. These effects may be mediated through activation of the AMPK/PGC-1α signaling pathway.
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EFFECTS OF SIALIC ACID INTERVENTION ON INTESTINAL FUNCTION IN AUTISM MODEL RATS

Yang Chao, Li Hongjie, Li Gang, Gao Yue, Chen Meiqi, Yang Xiaolei

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【Abstract】 Objective To explore the effects of sialic acid intervention during pregnancy and lactational period on the intestinal function of autism model rats. Methods Thirty SPF-grade adult male and female Wistar rats were mated. The successfully pregnant rats were randomly assigned to valproate induced model group (VPA group), high dose sialic acid group (SAH group), medium dose sialic acid group (SAM group), low dose sialic acid group (SAL group) and control group (CON group) (n=6 per group) and were housed individually in single cages. On the 12.5th day of pregnancy, the pregnant rats in the VPA group and the SA intervention groups were given a single intraperitoneal injection of 600 mg/kg of sodium valproate (VPA), while the pregnant rats in the CON group were given an equal amount of normal saline. The SA intervention period was from E12.5 to the 21st day after the offspring born. Subsequently, the feces of the offspring rats in each group were collected. The diversity and structure of the gut microbiota were detected by 16S rRNA sequencing. The intestinal transit speed of the rats in each group was detected by intragastric administration of carmine. The expression levels of intestinal-related neurotransmitters (substance P, enkephalin, 5-hydroxytryptamine, vasoactive intestinal peptide, glutamate, gamma-aminobutyric acid) in the blood of the rats in each group were detected by the ELISA method. Results High-dose SA intervention did not affect the diversity of the gut microbiota in the VPA-induced autism model rats, but it changed the structure of the gut microbiota and increased the abundance levels of Prevotella_NK3B31 group, Prevotella, Prevotella spp., Alloprevotella, Lachnospira, Ruminococcus, Bacteroides, etc. (p < 0.05). It promoted the intestinal transit speed of the model rats. Moreover, it increased the levels of vasoactive intestinal peptide, 5-hydroxytryptamine, and gamma-aminobutyric acid in the serum of the rats. Conclusion SA intervention during pregnancy and lactational period affects the intestinal transit speed of VPA-induced autism model rats, changes the structure of the gut microbiome, and increases the expression levels of vasoactive intestinal peptide, 5-hydroxytryptamine, and gamma-aminobutyric acid.
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Optimization of External Contract Management for Laboratory Animal Technology Services in Medical Research Institutes

wangyangyang, liujiangning

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In recent years, the demand for laboratory animals has been steadily increasing, leading to a rise in the number of external contracts signed by medical research institutes for laboratory animal technology services. Consequently, improving the management of these contracts has become a key focus. Drawing on the author’s practical experience in contract management, this article highlights five major issues in the current management of external laboratory animal technology service contracts in research institute ：1.Insufficient awareness of legal risks associated with contracts. 2.Lack of standardized contract templates, with ambiguous or missing terms.3.A disconnect between the departments responsible for contract execution and management.4.Insufficient professional qualifications among contract management staff.5.The unique nature of managing contracts for animal experimentation. To address these challenges, the article offers the following recommendations for improvement: 1.Strengthen the establishment of legal teams within research institutes and raise awareness of legal risks in contracts. 2.Improve the contract management system and increase staff motivation for more effective management. 3.Create an electronic information management platform for external laboratory animal technology service contracts. 4.Provide enhanced professional training for staff involved in managing these contracts. Hope Medical research institutes aim to implement these suggestions in their practices to optimize the management of laboratory animal technology service contracts in future. This will allow them to better support social scientific research and contribute to the advancement of national life sciences and technological innovation.
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Advancements in utilizing IPSC and gene editing technology to comprehend the genetic etiology underlying congenital heart disease

wangyuanyuan, xvhongyan, XIAOSHUOHUI, weifengxiang

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Congenital heart diseases (CHD) are the leading cause of mortality associated with birth defects. Significant advancements have been made in comprehending the genetics of CHD through Whole Genome Sequencing (WGS) and Whole Exome Sequencing (WES) technologies. Cell and animal models have emerged as reliable choices to gain insights into the specific genetic mechanisms and factors underlying CHD. Human induced pluripotent stem cells (iPSCs) offer a novel approach for studying CHD by generating patient-specific iPSC-derived cardiomyocytes for related research. The utilization of CRISPR-Cas9 gene editing tools enables the introduction or correction of variant genes in iPSCs, facilitating a more comprehensive exploration of variant pathogenicity and molecular basis in CHD. In this review, we discuss the genetic progress achieved through genome sequencing in relation to CHD while also exploring how gene editing techniques and patient iPSCs contribute to our understanding of the genetic mechanisms underlying CHD. We highlight the significance of combining these two approaches for disease research, providing valuable insights for clinical investigations on the mechanism behind CHD.
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Comparative study on the effects of imiquimod and cyclophosphamide in inducing alopecia areata model in C57 mice

renzhenni

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【Abstract】Objective To establish a C57BL/6J mouse model of alopecia areata (AA) induced by imiquimod (IMQ) and cyclophosphamide (CTX) and compare its characteristics. Methods 104 C57BL/6J mice were divided into an IMQ group (applying 5% 0.05 g IMQ to the head/back, 4 times a week, for 4 weeks) and a CTX group (intraperitoneal injection of 3 mg/20 g CTX after hair removal). The control group was treated with Vaseline (0.05 g) or only hair removal in the corresponding area. During the modeling process, continuously monitor the changes in body weight and hair of mice. HE staining was used to observe changes in skin hair follicles and epidermal thickness. The Elisa method was used to detect the levels of interferon - γ (IFN-γ), interleukin-15 (IL-15), and tumor necrosis factor - α (TNF-α) in mouse head and back skin lesions and serum. Results The IMQ modeling cycle is about 4 weeks, and in the fourth week, a patchy bare area with an area of about 1 cm × 1 cm is formed at the head and back skin lesions, accompanied by a small amount of scales; The modeling cycle of CTX is about 14 days. After intraperitoneal injection of CTX for 5 days, the hair on the head and back lesions falls off, and the skin appears dark gray. Histopathology showed significant changes in hair follicles between the two model groups of mice compared to the control group, with the IMQ model group showing more significant thickening of the epidermis. Both IMQ and CTX modeling methods can significantly increase IFN-γ, IL-15, and TNF-α in skin tissue and serum, with the IMQ modeling method showing a more pronounced increase in inflammatory factors. Conclusions Both IMQ and CTX can successfully induce alopecia areata models in the head and back of C57BL/6J mice. Compared with IMQ modeling, CTX modeling has the advantages of shorter modeling time, higher survival rate, and higher modeling rate, making it a relatively stable AA animal modeling method.
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Role of HIF-1α/VEGF signaling pathway in ischemic stroke and research progress in traditional Chinese medicine interventions

wangsenyu, liuxiangzhe, machiyuan, ranchunlong

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Ischemic stroke represents one of the most prevalent major chronic cerebrovascular diseases. The HIF-1α/VEGF signaling pathway serves as a crucial mediator of angiogenesis and has demonstrated bidirectional regulatory characteristics in ischemic stroke treatment through multifaceted mechanisms involving angiogenesis modulation, neurogenesis, oxidative stress regulation, inflammatory response control, and autophagy modulation. Emerging evidence indicates that traditional Chinese medicine exerts therapeutic effects on ischemic stroke by targeting the HIF-1α/VEGF pathway, effectively ameliorating oxidative stress, inflammatory reactions, cellular autophagy, and apoptosis while promoting vascular regeneration in ischemic regions. This review systematically elucidates the dual-phase regulatory mechanisms and functional characteristics of the HIF-1α/VEGF signaling pathway in ischemic stroke pathogenesis and progression. Furthermore, it comprehensively summarizes recent advancements in TCM-based interventions targeting this pathway, aiming to provide evidence-based theoretical support and clinical references for optimizing therapeutic strategies against this debilitating neurological disorder
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Research progress of oncolytic virus in tumor immunogenic cell death

zhangsibo, jialifang, lilulu, wangjing, liukaiyang

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Immunogenic cell death (ICD) is a special cell death mode that can activate the immune system, especially in the treatment of cancer. ICD can enhance the recognition and attack of the immune system on tumors by releasing a series of damage associated molecular patterns (DAMPs), so as to achieve the effect of killing tumors. Oncolytic virus (OV) is a kind of virus that can selectively infect and kill tumor cells while preserving normal cells from damage. OVs, as type II ICD inducers, induce ICD in tumor cells by targeting the endoplasmic reticulum. Based on the characteristics of ICD, this review further elaborated the mechanism of ICD induced by OVs and the latest clinical progress, providing some ideas and references for the future treatment of tumors.
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Effect of osteopontin (OPN) interference on Warburg effect ofhepatoma cells and its mechanism

lin ting, An riwen, Zhao fangxi, Qu lei, Fan wenxuan, Wu jianqiang, Zhang xuan

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Objective To investigate the effect of osteopontin (OPN) interference on the Warburg effect of hepatoma cells and the related molecular mechanism. Methods Small interfere RNA (siRNA) targeting OPN (si-OPN) and negative control (si-NC) were transfected into HepG2 and SK-HEP-1 cells. 2-NBDG fluorescent probe was used to detect the glucose uptake capacity of hepatoma, and the lactate detection kit was used to evaluate the lactate production in HepG2 and SK-HEP-1 cells. The expression of glycolysis-related genes, suchas GLUT1, HK2 and LDHA was assessed by RT-qPCR and western blot assays. After silencing the expression of LGALS3BP in HepG2 and SK-HEP-1 cells, Western blot was used to detect the expression of LGALS3BP, GLUT1, HK2 and LDHA. The glucose uptake and lactate production were also evaluated in LGALS3BP silenced HepG2 and SK-HEP-1 cells. Results Compared with the control group and si-NC group, the levels of glucose uptake and lactate production were significantly reduced in HepG2 and SK-HEP-1 cells interfe
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Establishment of a Method for Detecting FABP4 Gene Expression Levels in Macaca fascicularis

yang ru jia, wang chen yun, li yong jie, long wei hu, li zhe li, ye you song, yang wan jing, li ming hao, tang dong hong

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Objective To establish a method for detecting the mRNA expression level of FABP4 gene in Macaca fascicularis. Methods Six pairs of real-time quantitative PCR(RT-qPCR) primers were designed according to the mRNA sequence of fat FABP4 gene. Adipose tissue of Macaca fascicularis was collected in vivo; total RNA was extracted and reversely transcribed into cDNA. The designed 6 pairs of primers were used for RT-qPCR detection. According to the amplification curve and melting peaks, the primers with the most sensitive detection and without non-specific amplification were selected. The standard curve of gene expression was constructed by 100, 10-1, 10-2, 10-3, and 10-4times diluted cDNA. Two groups, namely the young and old groups of Macaca fascicularis, were established to validate the real-time fluorescence quantitative PCR detection method for the expression of the FABP4 gene in Macaca fascicularis adipose tissue. Results A pair of primers with the highest detection sensitivity were screened out, and a real - time fluorescence quantitative PCR method for detecting the expression level of FABP4 gene in Macaca fascicularis adipose tissue was established. The relative expression of the FABP4 gene in the adipose tissue of crab-eating macaques is higher in the elderly group compared to the young group . Conclusion A real-time quantitative PCR method has been successfully established for detecting the transcriptional levels of the FABP4 gene in the Macaca fascicularis.
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Effect of human milk on serum bilirubin and intestinal microbiota in neonatal jaundice rats

Peng qian, Zhang Heng, Jiang shi cheng, Luo ke yong, Duan miao

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Objective To investigate the effects of human milk on serum bilirubin levels and gut microbiota in neonatal rats with hyperbilirubinemia. Methods A total of 24 7-day-old SPF SD rats were randomly divided into 4 groups: bilirubin and normal saline were injected respectively, and 24 hours later, human milk or formula milk were administered for intervention, human milk-normal saline group (HN), human milk-bilirubin group (HB), formula milk-normal saline group (FN), and formula milk-bilirubin group (FB), samples were taken 72 hours later, and serum bilirubin values were detected by ELISA. 16S rDNA high-throughput sequencing was used to analyze intestinal microbiota. Results There were significant differences in the composition of intestinal microbiota between human milk and formula milk after gatric administration, and Firmicutes, Enterococci and Staphylococcus were the main microbiota in the HN group and HB group, while Proteobacteria, Escherichia coli-Shigella and Acinetobacter were the main ones in the FN group and FB group. There was no significant difference in bilirubin value between the groups, Pseudomonas was negatively correlated with indirect bilirubin value. Conclusion Changes in the structure of the intestinal microbiota in human milk and formula feeding, and Pseudomonas may be associated with bilirubin.
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Mechanistic investigation of Catalpol-Paeoniflorin in promoting neural stem cell proliferation and migration via miR-124 inhibition for perimenopausal depression treatment

SONG Lei, MAO Si-Yu, CAO Xiao-Jing

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Objective：To investigate the ameliorating effect of catalpa alcohol-paeoniflorin (CTP-PNF) on perimenopausal depression (PMD) and its potential mechanism by inhibiting miR-124 to promote the proliferation and migration of neural stem cells. Methods : The intervention effect of CTP-PNF was systematically evaluated by establishing a human-derived PMD mouse model, using brain-localized microinjection of miR-124 inhibitor/control, and in vitro fetal mouse neural stem cell extraction and transfection experiments. Sucrose preference test (SPT), tail suspension test (TST) and new environment food suppression test (NSFT) were used to detect depressive-like behaviors in mice. qRT-PCR was used to detect the expression of miR-124 in mouse prefrontal cortical tissues. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of norepinephrine (NE), dopamine (DA), serotonin (5-HT) and γ-aminobutyric acid (GABA) in serum and prefrontal cortex. Nissl staining was used to detect the pathological status of neurons in the prefrontal cortex and hippocampus. MTT was used to detect cell viability. Transwell assay to test migration capability; Network pharmacology was used to comprehensively analyze the common targets of miR-124-mediated CTP-PNF intervention in PMD, and the protein-protein interaction network was established, and the David platform was used for gene ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis. Results: The results showed that compared with the model group, CTP-PNF could significantly improve the depressive-like behavior and reduce the expression of miR-124 in the prefrontal cortex (P<0.001). Inhibition of miR-124 expression reduced depression-like behavior, increased the content of neurotransmitters (P<0.05), and improved nerve damage in the prefrontal cortex and hippocampus. The intervention of CTP-PNF medicated serum and the silencing of miR-124 can improve the vitality of neural stem cells, enhance their migration ability, and promote neural stem cell repair. Comprehensive bioinformatics analysis of network pharmacology showed that miR-124-mediated CTP-PNF treatment of PMD mainly involved 56 core therapeutic targets, and its key pathways included "hypoxia-inducible factor 1 signaling pathway", "serotonergic synaptic signaling pathway" and "cAMP signaling pathway" related to MAPK1, STAT3, TP53 and VEGFA. Conclusions: This study confirms that CTP-PNF significantly ameliorates depressive-like behaviors and neuropathological damage in perimenopausal depression mice by downregulating miR-124 to promote neural stem cell proliferation/migration and regulate neurotransmitter networks. Its effects involve multiple signaling pathways including hypoxia-inducible factor 1 and serotonergic synapse, providing a novel TCM intervention strategy and molecular targets for treating perimenopausal depression.
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Application of Artificial Intelligence in Predicting and Diagnosing Heart Failure

wangyadong, jiafuyun, liusirui, zhangrui, qiguangwei, xuqiang

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Heart failure (HF) is a disease with high incidence rate and high mortality rate worldwide. Artificial intelligence (AI) is increasingly used in the cardiovascular field. This article summarizes the application and research progress of the combination of artificial intelligence technology and clinical examination methods in the prediction and diagnosis of heart failure based on the current status of AI. AI identifies the contraction of the heart chamber, evaluates the structure of the heart, and predicts heart failure by learning parameters from echocardiography. The electrocardiogram model established by AI has higher agility in predicting heart failure than clinical doctors; The new biomarkers and genetic genes discovered by artificial intelligence can guide the prediction and diagnosis of heart failure and the screening of high-risk populations. They can also identify the risk of heart failure and prevent its occurrence by learning other disease characteristics. Artificial intelligence technology has the advantages of convenience, reliability, and high efficiency in the early diagnosis of heart failure, providing new possibilities and challenges, and further guiding treatment and prognostic care.
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Zhejiang's Practices and Reflections on the "Separation of Permits and Certificates" Reform in Laboratory Animal Licensing

huhuiying, wufang, kexianfu

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This paper examines the current status of Zhejiang Province’s laboratory animal industry following the implementation of the license separation reform. The study reveals that while the reform has lowered market entry barriers and increased the number of market entities, it has also introduced new challenges to the regulatory system. Both the production and use of laboratory animals have expanded, with quality improvements observed, yet issues of insufficient standardization persist. Although scientific research and innovation capabilities have improved, regional development disparities remain evident. To address these challenges, the paper proposes countermeasures such as refining the regulatory framework, strengthening industry self-regulation, and enhancing scientific research and innovation capabilities, aiming to foster the healthy development of Zhejiang’s laboratory animal industry.
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Research on the anti-myocardial ischemia reperfusion injury effect and mechanism of hawthorn based on HIF-1 signaling pathway

luoxiaoquan, SHU Kun, LUO Tao, ZHANG Xianyan, ZENG Caihua

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Objective:To investigate the protective effects and mechanisms of hawthorn extract against myocardial ischemia-reperfusion (I/R) injury in rats via the HIF-1 signaling pathway.Methods :An ex vivo rat heart I/R model was established. Animals were randomized into five groups: Sham, I/R, low-dose hawthorn flavonoids (HTF-L), high-dose hawthorn flavonoids (HTF-H), and HTF-H combined with the PI3K inhibitor LY294002. Cardiac function (LVSP, LVEDP, ±dp/dt_max), myocardial apoptosis (TUNEL), oxidative stress markers (SOD, MDA), and protein expression of HIF-1α and upstream pathways (PI3K/Akt, MAPK) were assessed after 60 min reperfusion.Results:Compared with Sham, I/R led to significantly impaired cardiac function, increased apoptosis, and oxidative stress. HTF treatment markedly improved cardiac function and suppressed apoptosis and oxidative stress in a dose-dependent manner. Western blot showed that HTF upregulated HIF-1and upstream signaling proteins; PI3K inhibition partially reversed these effects.Conclusion:Hawthorn extract attenuates myocardial I/R injury in rats, likely through activation of the HIF-1 pathway, reduction of apoptosis, and oxidative stress. These findings support the use of hawthorn in cardiovascular protection and provide mechanistic insights.
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Exploring the molecular mechanism of isorhamnetin against liver fibrosis based on network pharmacology and Mendelian randomization

zhengyang, yang shiquan

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Abstract: Objective: To investigate the mechanism and core targets of isorhamnetin in preventing and treating liver fibrosis. Methods: Bioinformatics data were integrated to identify liver fibrosis-related targets via differential gene analysis and weighted gene co-expression network analysis (WGCNA). Key intersecting targets with isorhamnetin's action targets were screened. Machine learning optimized core targets, validated for causal association using Mendelian randomization (MR). Molecular docking and dynamics simulations assessed target function. Results: 113 interactive targets of liver fibrosis and isorhamnetin were identified, primarily enriched in PI3K-AKT, TNF, and other signaling pathways. Machine learning combined with MR pinpointed AHR, CASP3, and MAPK14 as core targets. Multi-dataset validation confirmed their consistent expression and significant diagnostic efficacy (AUC >0.7). Molecular simulations demonstrated stable binding of isorhamnetin to these targets (binding energy < -7.0 kcal/mol). Conclusion: Isorhamnetin inhibits liver fibrosis by targeting AHR, CASP3, and MAPK14 to regulate inflammation, apoptosis, and metabolic pathways. This study provides novel insights into the anti-fibrotic mechanisms of traditional Chinese medicine components.
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Effect of butorphanol on lipopolysaccharide induced chondrocyte injury by regulating SDF-1α/CXCR4 pathway

Fang jun

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Objective: To discuss the effect of butorphanol on lipopolysaccharide induced chondrocyte injury and analyze whether its mechanism is related to the stromal cell-derived factor-1α (SDF-1α)/C-X-C chemokine receptor 4 (CXCR4) pathway. Methods: Human chondrocytes C28/I2 were cultured in vitro and assigned into control group (normal culture), model group (100 μmol/L lipopolysaccharide), model+low-dose butorphanol group (100 μmol/L lipopolysaccharide+1 μmol/L butorphanol), model+medium-dose butorphanol group (100 μmol/L lipopolysaccharide+2 μmol/L butorphanol), model+high-dose butorphanol group (100 μmol/L lipopolysaccharide+4 μmol/L butorphanol), and model+high-dose butorphanol+NUCC-390 group (100 μmol/L lipopolysaccharide+4 μmol/L butorphanol+500 nmol/L CXCR4 agonist NUCC-390). MTT assay, ELISA assay, flow cytometry, and western blot were used to detect cell viability, the IL-6 and TNF-α levels, the cell apoptosis, apoptosis, and the SDF-1α/CXCR4 pathway related proteins, respectively. Results: For the control group, the model group showed decreased chondrocyte survival rate and Bcl-2 protein, and increased TNF-α, IL-6, apoptosis rate, Bax, Cleaved caspase-3, SDF-1α, and CXCR4 proteins (P<0.05). For the model group, the model+low, medium, and high-dose butorphanol groups showed increased chondrocyte survival rate and Bcl-2 protein, and decreased TNF-α, IL-6, apoptosis rate, Bax, Cleaved caspase-3, SDF-1α, and CXCR4 proteins (P<0.05). For the model+high-dose butorphanol group, the model+high-dose butorphanol+NUCC-390 group showed decreased chondrocyte survival rate and Bcl-2 protein, and increased TNF-α, IL-6, apoptosis rate, Bax, Cleaved caspase-3, SDF-1α, and CXCR4 proteins (P<0.05). Conclusions: Butorphanol may improve chondrocyte injury induced by lipopolysaccharide by inhibiting SDF-1α/CXCR4 signaling pathway.
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Analysis of Characteristics of Animal Models for Acute Kidney Injury Based on Data Mining

Zhang Fenfen, Qin Lei, Chen Jiali, Chen Lei, Zhang Delin, Cheng Shaomin

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Objective To summarize the characteristics of animal models of acute kidney injury (AKI) both domestically and internationally, providing references for the standardization and normalization of animal model preparation for this disease. Methods We searched and collated relevant literature on AKI animal models included in CNKI, Wanfang, VIP, SinoMed, and PubMed databases since their establishment. Data statistics and analysis were conducted on animal strains, modeling methods, modeling cycles, modeling criteria, positive drugs, detection indicators, and other contents. Results A total of 266 articles were included (220 in Chinese and 46 in English). The majority of animal strains were male rats, aged 8 to 10 weeks and weighing 180 to 250 g. There were 22 modeling methods, primarily consisting of ischemia-reperfusion and intramuscular injection of glycerol as single-factor modeling approaches. The modeling cycle was mostly concentrated within 14 days, with the highest number of articles recording between 6h to 24h. The criteria for establishing the model were not fully unified, but most articles judged based on SCr, BUN, and renal pathological changes. Positive drugs mainly included captopril and ginsenoside. Detection indicators mainly involved comprehensive evaluations such as renal function assessment, histopathological evaluation, and experimental animal observation. Conclusion Currently, there is still a lack of well-standardized AKI animal model preparation and modeling criteria with high clinical concordance. The comprehensive application of multi-level and multi-angle detection indicators needs improvement. There remains significant research space for establishing a combined model of traditional Chinese medicine syndromes and diseases
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Application Analysis of Animal Models of Crohn’s disease Based on Data Mining

WU Yue, HE Youcheng, MO Lian, CAI Shuyu, JIANG Fengru, ZHOU Chunyu, PAN Keyi, YUAN Jianye

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Objective To summarize and analyze the current status of animal models for Crohn"s disease (CD) based on literature data mining, providing insights for optimizing the preparation methods and evaluation criteria of CD animal models. Methods Literature related to CD animal models was retrieved from the China National Knowledge Infrastructure (CNKI), Wanfang Data, and PubMed databases. Information on animal species, modeling methods, detection indicators, and positive intervention strategies was extracted. A database was established using Excel software for statistical analysis. Results A total of 411 eligible Chinese and English articles were included. The majority of CD animal models utilized 6-8-week-old SD rats, C57BL/6J mice, or BALB/c mice, predominantly male. Modeling methods comprised six categories: chemical induction (primarily TNBS), genetic engineering (e.g., IL-10－^/－^,TNF△^ARE mice), spontaneous models, immune-mediated models, microbial colonization, and combination approaches. Detection indicators encompassed general phenotypic characteristics, pathological alterations, inflammatory markers, intestinal permeability, intestinal fibrosis, immunological changes, gut microbiota and metabolite profiles, and signaling pathways. Among positive interventions, biological agents were most frequently employed in Western medicine, while acupuncture was predominant in traditional Chinese medicine. These models were widely applied in drug efficacy evaluation, mechanism exploration, and novel model development. Conclusion Current CD animal models employ diverse preparation strategies, simulating multiple dimensions of CD characteristics and aligning well with Western medical criteria. Based on this data mining analysis, future research should focus on establishing standardized modeling protocols and developing integrated animal models that incorporate disease and syndrome features from both traditional Chinese and Western medicine, while encompassing the full disease progression of CD. Such advancements will enhance research reliability and accelerate investigations into pathogenesis and innovative therapeutic development.
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Research Advances in Mitochondrial Quality Control Dysfunction and Glandular Damage in Sj?gren"s Syndrome

WANG Yue, MENG Xiangyu, WANG Mengjie, LIU Ying

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Sjogren's syndrome (SS) is a chronic autoimmune disease with complex pathogenesis. In addition to lymphocyte infiltration and inflammatory damage of the glands，it often involves multiple systems，but the treatment options are limited. Studies have found that mitochondrial quality control dysfunction is closely related to the inflammation of autoimmune diseases. This article aims to study the correlation between mitochondrial quality control dysfunction and glandular damage in SS，with a view to broadening the horizons for the treatment of SS.
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LCMT1 knockout regulates lipid metabolism to alleviate fructose-induced lipid deposition in primary hepatocytes

LI Huilian, LAN Li, WANG Xinhang, LI Xiaoman, LONG Yijin, WANG Minghong, LU cailing, LI Xiyi, TANG Shen

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Objective　To investigate the effect of leucine carboxyl methyltransferase 1 (LCMT1) knockout on fructose-induced lipid deposition in primary mouse hepatocytes. Methods　Primary hepatocytes were isolated from wild-type (WT) and hepatocyte-specific LCMT1 knockout (KO) mice via a two-step hepatic portal vein perfusion method. The cells were divided into four groups: WT-Control, WT-5 mmol/L fructose, KO-Control, and KO-5 mmol/L fructose. Cell viability was determined by Alamar-Blue. Hepatocyte injury was evaluated by measuring alanine aminotransferase and aspartate aminotransferase levels. Lipid deposition was visualized via Oil Red O staining and lipid droplet green fluorescence staining, whereas the cellular triglyceride content was quantified via a GPO-POD assay kit. The mRNA expression of lipid metabolism-related genes was detected via quantitative real-time PCR, and the protein expression of LCMT1 and PP2Ac was detected via Western blotting. Results　Fructose treatment did not significantly alter cell viability in any group, and no significant cell damage was observed (P > 0.05). Compared with the WT-Control group, the WT-5 mmol/L fructose group presented marked accumulation of lipid droplets in hepatocytes (P < 0.001), with significantly elevated triglyceride content (P < 0.05). The mRNA levels of the de novo lipid synthesis genes ChREBP, SREBP-1c, and ACC1 were increased (P < 0.05, P < 0.001, P < 0.001), whereas FAS expression was not significantly altered (P > 0.05). The mRNA levels of the lipid uptake genes FABP1 and FATP2 were also significantly increased (P < 0.05, P < 0.05). In contrast, the KO-5 mmol/L fructose group presented a reduced number of lipid droplets (P < 0.01, P < 0.001), decreased triglyceride content (P < 0.05), and downregulated mRNA levels of ChREBP, SREBP-1c, ACC1, FABP1, and FATP2 (P < 0.01, P < 0.001, P < 0.001, P < 0.001, P < 0.05). In contrast, CPT1 mRNA levels were markedly increased (P < 0.01). Compared with that in the WT-Control group, the total expression of PP2Ac was significantly greater (P < 0.05), and PP2Ac demethylation was significantly lower (P < 0.01) in the WT-5 mmol/L fructose group. In the KO-Control group, total PP2Ac expression remained unchanged (P > 0.05), whereas PP2Ac demethylation was markedly elevated (P < 0.001). Compared with the WT-5 mmol/L fructose group, the KO-5 mmol/L fructose group presented markedly decreased total PP2Ac expression and significantly elevated PP2Ac demethylation levels (P < 0.05, P < 0.01). Conclusion　LCMT1 knockout alleviates fructose-induced lipid deposition in primary hepatocytes by inhibiting lipid uptake, enhancing fatty acid oxidation, and downregulating de novo lipid synthesis. This mechanism involves LCMT1 knockout-mediated upregulation of PP2Ac demethylation, thereby modulating PP2A activity.
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Study on the technical comparison and pedagogical application of arrhythmia model based on barium chloride rabbit model and Wabaine guinea pig model

rao yuliang, MA Shulan, ZHANG Yadong, YAN Yufeng

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Objective The purpose of this study was to compare and analyze the barium chloride-induced arrhythmia model in rabbits with the wowbaine-induced arrhythmia model in guinea pigs, to provide technical references for medical experimental teaching, and to improve the electrophysiological experimental skills of medical students. Methods A systematic comparative analysis of the two models was conducted from the dimensions of technical principle, modeling method, and index detection. By optimizing the electrocardiographic parameters, standardizing the arrhythmia grading criteria and introducing quantitative analysis methods, we explored the differences between the two models in terms of ion channel mechanisms, drug targets and applicability to teaching. Results The barium chloride model can rapidly induce ventricular arrhythmia and is suitable for acute drug efficacy observation; the wowbaine model can simulate progressive arrhythmia development and is suitable for the study of preventive effects of antiarrhythmic drugs. Conclusion This study provides a basis for the selection, process optimization and mechanism understanding of arrhythmia models in medical experimental teaching, which is of great significance for improving electrophysiology experimental skills of medical students.
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Research progress in the regulation and treatment of Parkinson’s disease by the AMPK signaling pathway

sunchenfeng, renbinbin

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Parkinson"s disease (PD), the second most common neurodegenerative disorder, involves dopaminergic neuron degeneration, abnormal α-synuclein aggregation, and energy metabolic disruption. AMP-activated protein kinase (AMPK), a key cellular energy metabolic regulator, has multiple roles in PD progression. This paper explores AMPK"s structure and function, and its regulatory mechanisms in PD, such as modulating neuronal energy metabolism, mediating mitochondrial function, inhibiting oxidative stress, inducing autophagy, and regulating neuroinflammation and apoptosis. It also reviews potential AMPK-based PD therapies, including natural products (resveratrol, curcumin, etc.), gene therapy, and targeted delivery systems, while noting the need to precisely control AMPK"s dual effects (e.g., overactivation causing energy stress). Future research should focus on AMPK"s interactions with other pathways (e.g., SIRT1, NF-κB) and improving the spatiotemporal specificity of targeted treatments for clinical translation. This study offers crucial theoretical support for understanding PD mechanisms and developing AMPK-targeted therapies.
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Research progress of traditional Chinese medicine regulating GR/ NF-κB /NLRP3 signaling pathway in the treatment of depression

Yan DI, Tian Ruihan, Li Yuexin, Zhang Zhijing, Guo Ziyi, Liu Wentao, Du Zhixin, Lu Jincan, Hu Xueyan, Yao Jianping

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Major Depressive Disorder (MDD) is one of the main causes of suicide. Monoamines, the mainstay of treatment for the disease, have limited efficacy, highlighting the urgent need for improved treatment. Traditional Chinese medicine (TCM) has shown the advantages of multiple mechanisms of action and fewer side effects in this field, which has become a potential treatment option. In recent years, the important regulatory role of GR/NF-κB/NLRP3 signaling pathway in the treatment of depression has gradually attracted attention. Studies have shown that this signaling pathway is mainly closely related to the hypothalamic-pituitary-adrenal axis, the inhibition of neuroinflammation and the regulation of nerve cell pyroptosis. This article reviews the mechanism of traditional Chinese medicine"s antidepressant effect by regulating GR/NF-κB/NLRP3 signaling pathway, in order to provide theoretical basis for the treatment and further research of depression.
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Progress in the Biological Mechanisms of Pigeon Geomagnetic Navigation

ZHAO Yong, WANG Fang, WU Pengpeng, SHI Changhong

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Homing pigeons and many other animals have exquisite geomagnetic sensing ability, and can accurately find the appropriate path and direction during the long migration route, which is the preferred model animal for the study of biological geomagnetic navigation. Although bio-geomagnetic navigation has made great progress in the past few decades, its biological mechanism is still unclear. In this paper, we review the recent advancements in the research of biological magnetoreception using homing pigeons. It focuses on the magnetic sensing mechanisms of the magnetoreceptor models based on nanoscale ferromagnetic particles and the radical pair model induced by light. It also proposes the key directions that future biological magnetoreception research should focus on. It is expected to provide more theoretical basis for the study of geomagnetic navigation using homing pigeons and help reveal the operating principles of the biological magnetic perception system.
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Knockdown of GBA inhibits the malignant progression of DDP-resistant ovarian cancer cells by regulating EGFR signaling pathway

Dai xiao yan

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Objective: The purpose of this study was to investigate the effect of β-glucosidase (GBA) knockdown on the malignant progression of cisplatin (DDP) -resistant ovarian cancer cells, and to explore the mechanism of its regulation of epidermal growth factor receptor (EGFR) signaling pathway. Methods: A2780/DDP cells were divided into three groups: Con group (blank control), si-NC group (transfected with negative control si-NC), si-GBA group (transfected with si-GBA) and NSC 228155 group ( transfected with si-GBA and treated with 2 μmol/L NSC 228155 ). The protein expression levels of GBA, E-cadherin, N-cadherin, Vimentin, EGFR, p38 MAPK, phosphorylated (P)-p38 MAPK, ERK and (P)-ERK were detected by Western blot. The expression of GBA was measured by RT-qPCR in relative terms. To evaluate the cellular proliferative activity, migratory potential, and invasive capacity, we conducted CCK-8 proliferation assays, plate clonogenic assays, scratch wound healing assays, and Transwell migration tests. Results: Compared with the A2780 group, the protein expression level and mRNA relative expression of GBA in the A2780/DDP group were significantly increased (P<0.05). Compared with Con group and si-NC group, the proliferation activity, the number of cloned cells, the number of cloned cells and the number of transmembrane cells in si-GBA group were significantly decreased (P<0.05). There was a significant increase in the expression of E-cadherin (P<0.05), accompanied by a notable decrease in the expression levels of Vimentin, N-cadherin, and EGFR (P<0.05). Additionally, the ratios of phosphorylated p38 MAPK to total p38 MAPK (P-p38 MAPK/total p38 MAPK) and phosphorylated ERK to total ERK (P-ERK/total ERK) also exhibited significant downregulation (P<0.05). Compared with si-GBA group, the proliferation activity, the number of cloned cells, the number of cloned cells and the number of transmembrane cells in NSC 228155 group were significantly increased (P<0.05). A notable decrease was observed in the expression of E-cadherin (P<0.05), whereas there was a significant upregulation in the expression levels of Vimentin, N-cadherin, and EGFR (P<0.05). Additionally, the ratios of phosphorylated p38 MAPK to total p38 MAPK (P-p38 MAPK/p38 MAPK) and phosphorylated ERK to total ERK (P-ERK/ERK) also demonstrated a marked increase (P<0.05). In the nude mouse xenograft experiment, compared with the blank control group, the volume and weight of the transplanted tumor in the blank control+DDP group were significantly reduced (P<0.05). In comparison to the negative control group, a statistically significant reduction was observed in both the volume and weight of the transplanted tumors in the group that received DDP in addition to the negative control+DDP group (P<0.05). Compared with the knockdown group, the volume and weight of transplanted tumors in the knockdown+DDP group were significantly reduced (P<0.05). In contrast to both the blank control group and the negative control group, the knockdown group exhibited a statistically significant reduction in both the volume and weight of the transplanted tumors (P<0.05). Similarly, when compared to the blank control+DDP group and the negative control+DDP group, the knockdown+DDP group demonstrated a notable decrease in the volume and weight of the transplanted tumors (P<0.05). Conclusion: The knockdown of GBA significantly inhibits the proliferation, migration, and invasion of DDP-resistant OC)cells, and suppresses the growth of subcutaneous xenografts of A2780/DDP cells in nude mice. The mechanism may be achieved by inhibiting the EGFR/MAPK/ERK signaling pathway.
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PGC-1α and TFAM in age-dependent ovarian decline in mice

ZHU Chenge, LU Ge, YIN Yaoli, LI Hongxiao, SHEN Meihong

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Objective To explore the characteristics and molecular mechanisms of ovarian function decline in naturally aging mice. Methods Eighteen female ICR mice of 2, 6, 10 and 14 months of age were included in the study, and the estrous cycle, ovarian index, pregnancy rate and embryo number were detected; the number of follicles was observed by HE staining; serum anti-Müllerian hormone (AMH) level was measured by ELISA; the protein and mRNA expression of P16, P21, proliferatoractivated receptor-γ coactivator-1α (PGC-1α) and mitochondrial transcription factor A (TFAM) were detected by IHC and qPCR respectively, and the protein expression of PGC-1α and TFAM was detected by Western Blot; Spearman"s rank correlation analysis and logistic regression analysis were used to assess the associations among indicators. Results Compared with the 2M group, the percentage of estrous cycle disorders (P<0.05 in the 10M group, P<0.01 in the 14M group), ovarian index (P<0.05 in the 10M group, P<0.01 in the 14M group), serum AMH level (P<0.01 in the 10M group, P<0.01 in the 14M group), the number of embryos (P<0.01 in the 10M group, P<0.01 in the 14M group), and the pregnancy rate (P<0.01 in the 14M group) were significantly decreased; the number of follicles at all levels and the total number of follicles were decreased (P<0.01 in each group), and the number of atretic follicles (P<0.01 in each group) was increased; the expression of P16 and P21 mRNAs (P16: P<0.01 in the 10M and 14M groups; P21: P<0.05 in the 10M group, P<0.01 in the 14M group) and proteins (P16: P<0.01 in each group; P21: P<0.01 in the 10M and 14M groups) were elevated; Spearman"s correlation analysis showed that the age in months was negatively correlated with the ovarian index, serum AMH level, primordial follicle number, number of embryos, and the expression of PGC-1α and TFAM, and positively correlated with the expression of atretic follicle, P16, and P21 (all P<0.01); Logistic regression analysis showed that there was a significant negative correlation between the age in months and the pregnancy rate (P<0.01).PGC-1α mRNA was significantly decreased (P<0.01 in all groups), and TFAM mRNA was significantly decreased in the 10M and 14M groups (P<0.01); PGC-1α protein was significantly decreased in the 10M group (IHC: P<0.05; WB: P<0.01) and the 14M group (all P<0.01); TFAM protein was significantly decreased in the 6M, 10M, TFAM protein was significantly reduced in the 6M, 10M, and 14M groups (IHC: P<0.01; WB: P<0.01). Compared with the 2M group, the expression of PGC-1α and TFAM was positively correlated with ovarian index and serum AMH level, and negatively correlated with the expression of P16 and P21 (all P<0.01). Conclusions Ovarian function in mice declines progressively with months of age, as reflected by fewer follicles, reduced fertility, and up-regulation of aging markers, which may be associated with decreased expression of the mitochondrial biogenesis factors PGC-1α and TFAM.
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The mechanism of desensitization of sensory neuron TRPV1 induced by benign mechanical stimulation to reduce inflammatory response of synovial fibroblasts in KOA model

Li Zhang, Hua Zhang, Ping Li, Song Gao, Guangjuan Ke, Liuxin Qu

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Objective: To construct an isolated model of knee osteoarthritis (KOA), which is co-cultured by dorsal root ganglion (DRG) and fibroblast-like synoviocytes (FLSs). To investigate the effect mechanism of transient receptor potential vanilloid type 1 (TRPV1) desensitization of sensory neurons induced by benign mechanical stimulation and its alleviation of FLSs inflammatory response. Methods: DRG neuronal cells were identified by immunofluorescence method. The stress loading of DRG neurons was realized by FX-6000T cell stress system, and the effect of mechanical stress on the activity of DRG neurons was measured by CCK-8 method. The calcium flux of DRG neurons in each group was studied by flow cytometry. Transwell chamber and FLSs were used to establish a co-culture system. The contents of pro-inflammatory factors IL-1β, TNF-α and TGF-β in the supernatant were determined by ELISA. The gene and protein expression levels of TRPV1 and its desensitizing negative regulatory proteins PP2B, CaM, IL-1β, TNF-α, TGF-β and α-SMA in DRG neurons were detected by PCR and WB, respectively. Results: The Ca2+ ion flux in DRG neurons increased under inflammatory environment, and the medium and high intensity mechanical stimulation further increased the Ca2+ ion flux (P<0.05), but the high intensity finger pressure did not further increase the medium intensity Ca2+ ion flux (P>0.05). Moderate and high intensity benign mechanical stimulation up-regulated TRPV1 gene and protein expression of DRG neurons in inflammatory group (P<0.05), but down-regulated PP2B and CaM gene and protein expression; Moderate and high intensity benign mechanical stimulation decreased the contents of IL-1β, TNF-α and TGF-β in the supernatance of co-cultured cells (P<0.05), and down-regulated the gene and protein expressions of IL-1β, TNF-α, TGF-β and α-SMA in FLSs (P<0.05). Conclusion: Moderate and high intensity benign mechanical stimulation induced TRPV1 desensitization of rat sensory neurons, and inhibited FLSs inflammatory response through intercellular communication.
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Shexiang Baoxin Pill Attenuates Valvular Dysfunction in Rats by Regulating Ferroptosis

CHEN Zhihao, LAN Zhenzhen, LIU Xincan, LIU Luyao, JIAO Xueyan, ZHANG Yifan, CHEN Yun

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Objective To investigate the effects and underlying mechanisms of Shexiang Baoxin Pill (SBP) on valvular dysfunction in rats induced by wire injury. Methods A rat model of aortic valve injury was established using a standardized wire injury method. Animals were randomly divided into a control group, sham-operated group, model group, and SBP low-, medium-, and high-dose intervention groups. Aortic valve function was evaluated by echocardiography. Histopathological changes were assessed using hematoxylin-eosin (HE) and Masson's trichrome staining. Serum levels of lipid peroxides (LPO), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), and total iron were measured using biochemical assays. The expression levels of ferroptosis-related proteins (ACSL4, SLC7A11, GPX4) and osteogenic markers (RUNX2, BMP2) in valve tissues were detected by Western blotting and RT-qPCR. Results Compared to the model group, the SBP medium- and high-dose groups significantly increased the aortic valve orifice area (3.70±0.04 mm2 and 3.90±0.11 mm2 vs. 2.25±0.37 mm2, P<0.05), reduced the transvalvular pressure gradient (0.52±0.09 mmHg and 0.49±0.13 mmHg vs. 0.90±0.17 mmHg, P<0.05), and decreased the aortic valve peak flow velocity (68.83±4.98 cm/s and 63.61±11.43 cm/s vs. 87.14±11.22 cm/s, P<0.05). HE and Masson staining results demonstrated that SBP alleviated valve thickening and fibrosis (fibrotic area: 35.98±5.25% vs. 53.01±2.44%, P<0.05). Biochemical tests showed that SBP reduced serum levels of lipid peroxidation products (LPO and MDA) and total iron ions while increasing SOD and GSH levels (P<0.05). Western blot and RT-qPCR results indicated that SBP downregulated the expression of ferroptosis-related protein ACSL4 (P<0.05) while upregulating anti-ferroptosis proteins SLC7A11 and GPX4 (P<0.05) and inhibiting the expression of osteogenic molecules RUNX2 and BMP2 (P<0.05). Conclusion SBP may alleviate valve dysfunction induced by mechanical injury in rats by modulating oxidative stress and restoring iron homeostasis. These findings provide experimental evidence for the potential role of SBP in the early intervention of valvular disease. However, the precise active components, molecular targets, and clinical translation of SBP require further investigation.
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Research progress on extracellular vesicles of mesenchymal stem cells and Alzheimer"s disease

liusirui, wangyadong, chenzhiyi, hanjingxian, zhangxuezhu

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With the development of aging in the world, Alzheimer"s disease (AD) has become a disease that seriously jeopardizes human health. Given the complexity of the pathogenesis of AD, there is a lack of therapeutic options that can effectively intervene in the disease process. Mesenchymal stem cell-derived exosomes (MSC-Exosomes) have emerged from a new perspective in medicine due to their powerful regenerative properties and repair function. They are donor-derived, low immunogenicity, easy to store, natural carriers, and low risk of tumor formation, and have shown great potential in the treatment of AD and post-treatment rehabilitation. showing great potential. Based on this, this article introduces the pathological mechanisms of Alzheimer"s disease and the characteristics of MSC-Exos, and provides a detailed review of the role of MSC-Exos in the treatment of AD, including anti-inflammatory, immunomodulatory, and related signaling pathway modulation, and discusses the latest progress in related research, with the aim of providing a new direction for therapeutic approaches to Alzheimer"s disease.
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Construction and comparative study of animal models of influenza A virus transmission and infection

YUANXIANGZHONG, PENGDONGDONG, wangzhuole, liuke, LIMENG, LIYUHAN, liuxuewu, tangzining

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Objective To establish a model of indirectly induced respiratory tract infection in animals by influenza A (H1N1) and H3N2 subtypes viruses, to screen influenza virus transmission hosts, and to provide theoretical support for the clinical control of influenza viruses. Methods 50 BALB/c mice and 50 Hartley guinea pigs were randomly divided into 5 groups, which were normal control group, virus infection group 1, virus infection group 2, close transmission group 1, and close transmission group 2, with 10 animals in each group of each species. Mice in virus-infected group 1 and virus-infected group 2 were fed with influenza A (H1N1) and influenza A (H3N2) viruses via nasal drip, while guinea pigs in virus-infected group 1 and virus-infected group 2 were fed with influenza A (H1N1) and influenza A (H3N2) viruses via nasal drip; the animals in virus-infected group 1 were housed together with those in the close-transmission group 1:1 the following day, and the animals in virus-infected group 2 were housed together with those in the close-transmission group 1:1 the following day. Animals in virus infection group 1 were housed 1:1 with animals in close transmission group 1 the next day after infection, and animals in virus infection group 2 were housed 1:1 with animals in close transmission group 2 the next day after infection. On the 7th day, the lung function, viral titre and viral load of the nasal tissue, trachea and lung tissue of each group were measured, and the pathological changes of the trachea and lung tissue of the animals in the close transmission group were detected. Results Compared with the normal control group-mice, the viral titers and viral loads of nasal, tracheal and lung tissues of the virus-infected group 1 and 2-mice and the closely transmitted group 1 and 2-mice were significantly increased (P < 0.01), and the pathological scores of the trachea and lung tissues were significantly elevated (P < 0.01), and the FVC and FEV20 of the virus-infected group 1 and 2-mice were significantly decreased (P < 0.01); compared with the normal control group-guinea pigs, the FVC and FEV20 of the virus-infected group 1 and 2-mice were significantly decreased (P < 0.01). Compared with the normal control group-guinea pigs, the nasal tissue, trachea and lung tissues of virus-infected group 1 and 2-guinea pigs, and the nasal tissue, trachea and lung tissues of animals in the close transmission group 1 and 2-guinea pigs showed significant increases in viral titre and viral load (P < 0.01), significantly higher trachea and lung histopathological scores (P < 0.01), and significantly lower FVC and FEV200 (P < 0.01). Conclusion In this study, influenza A H1N1 and H3N2 subtypes influenza viruses were used to indirectly induce respiratory tract infections in mice and guinea pigs, respectively, and the models were evaluated in terms of animal lung function, respiratory viral titre, viral load and pathology. The animal model of indirect transmission of influenza viruses in the respiratory tract has certain limitations, in which influenza viruses are transmitted less efficiently among mice and more efficiently among guinea pigs, and the model is stable. This further confirms that guinea pigs have the characteristics of efficient replication and transmission of the virus..
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Mechanism of PD-L1 in regulating oral cancer metastasis based on Bioinformatics and In Vitro Experiments

WANG Tian, NIE Xiaocui, WANG Xiaotang, GAO Jiping, SONG Xiaona, SONG Guohua

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Objective To investigate the role and mechanism of PD-L1 in oral cancer metastasis based on TCGA and GEO databases. Methods The expression characteristics and clinical significance of PD-L1 in oral cancer were analyzed using the TCGA database. qRT-PCR was used to detect PD-L1 expression levels in different oral cancer cell lines. The effects of PD-L1 knockdown on the proliferation, migration, and invasion of oral cancer cells (CAL27 and SCC25) were evaluated via CCK-8 assay, wound healing assay, Transwell assay and Matrix gel invasion experiment. The interaction network between PD-L1 and functional genes of oral cancer patients was constructed by using STRING software and GEO database, and key pathways were screened through KEGG enrichment analysis. qRT-PCR was employed to validate the regulatory relationship between PD-L1 and key genes. Results TCGA data revealed that PD-L1 was highly expressed in oral cancer patients and correlated with lymph node metastasis. PD-L1 was also highly expressed in oral cancer cell lines. PD-L1 knockdown significantly inhibited the proliferation, migration, and invasion of Cal27 and SCC25 cells. KEGG analysis indicated that PD-L1 activates the JAK/STAT pathway by upregulating CXCL9 and CXCL10, thereby promoting STAT1 expression to regulate oral cancer metastasis. Inhibition of the JAK/STAT pathway further suppressed the proliferation, migration, invasion, and expression of STAT1, CXCL9, and CXCL10 in Cal27 and SCC25 cells. Conclusions PD-L1 may promote oral cancer cell proliferation, migration, and invasion by upregulating CXCL9 and CXCL10 to regulate the JAK/STAT pathway and enhance STAT1 expression, ultimately driving oral cancer growth and metastasis.
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Research progress of epigenetic mechanism in TCM prevention and treatment of Parkinson's disease

li chi yang, lan rui

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Parkinson's disease (PD) is a common progressive neurodegenerative disease mainly in the motor system. In recent years, some genetic factors and cellular mechanisms of Parkinson's disease have been discovered, and emerging evidence suggests that epigenetic modifications and phenomena play a very important role in the prevention and treatment of Parkinson's disease. Epigenetic modification mediates genetic and environmental interactions mainly through the complex interaction of DNA methylation, histone modification and non-coding RNA, thereby affecting different expressions in the absence of changes in DNA sequence. In this review, we introduce the epigenetic modification mechanisms involved in the pathogenesis of Parkinson's disease. Recent studies have found that traditional Chinese medicine can participate in the regulation of abnormal epigenetic modification in the treatment of Parkinson's disease, and traditional Chinese medicine has a unique advantage in the treatment of Parkinson's disease, with a multi-level and multi-target overall regulatory effect. Scholars at home and abroad have studied the intervention of Parkinson's disease by traditional Chinese medicine monomers, traditional Chinese medicine compound prescriptions, and appropriate traditional Chinese medicine techniques, which confirms that traditional Chinese medicine has a good prospect in improving symptoms and research for Parkinson's disease. This article reviews the mechanisms of epigenetics in Parkinson's disease, explores the role of traditional Chinese medicine in it, and aims to provide new ideas for the clinical treatment and drug development of Parkinson's disease through epigenetic intervention.
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Impact and Mechanism of Resveratrol on Myocardial Energy Metabolism in Exercise-induced Fatigue Rats

Hu Yulong, XU Shang, ZHANG Libing, JIN Qiguan, CHEN Xianghe

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Objective: To explore the effects and mechanisms of resveratrol on the improvement of cardiomicronic energy metabolism in exercise-induced fatigue rats. Methods: 48 healthy male SD rats of 6-8 weeks old were selected and randomly divided into blank control group (C), resveratrol administration group (R), exercise-induced fatigue group (E) and exercise-induced fatigue + resveratrol administration group (ER), with 12 rats in each group. The rats in group E and ER were weight-bearing 5% of body weight for 60 min per day and exercised 6 days per week for 6 weeks. Rats in group R and ER were gavaged with resveratrol at 50 mg/kg 1 hr after exercise. Results: Compared with C, E rats showed a significant increase in plasma levels of BUN and CK (P < 0.05, P < 0.05), a significant increase in the activity levels of CK-MB and cTnI (P < 0.01, P < 0.05), a significant decrease in the activity levels of myocardial cytochrome C oxidase (COX) and succinate dehydrogenase (SDH) activity levels were significantly lower (P < 0.01, P < 0.05), and mRNA expression levels of mitochondrial energy metabolism- related genes silent information regulator 1 (SIRT1), peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α), and estrogen receptor-related receptor α (ERRα) were significantly lower (P < 0.01, P < 0.01, P < 0.01). Compared with E, the serum levels of BUN and CK in ER rats showed a significant decrease (P < 0.05, P < 0.05), the activity levels of CK-MB and cTnI showed a significant decrease (P < 0.05, P < 0.05), the activity levels of myocardial COX and SDH showed a significant increase (P < 0.01, P < 0.05), and the SIRT1, PGC-1α and ERRα expression levels of mRNA were significantly increased (P < 0.05, P < 0.01, P < 0.01). Conclusion: Resveratrol can effectively activate the SIRT1/PGC-1α/ERRα signaling pathway, improve myocardial energy metabolism in exercise fatigued rats, and protect against myocardial injury.
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Research Progress on Cell Models of Sarcopenia

SHI Yiting, ZHAO Peiyuan, LIU Xihong, GAO Gai, ZHANG Xiaowei, XIE Zhishen, ZHANG Zhenqiang

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Sarcopenia is a systemic disease characterized by accelerated loss of skeletal muscle mass and function, leading to an increased incidence of adverse outcomes such as falls and fractures. Sarcopenia is classified into primary and secondary types, with primary sarcopenia being closely related to aging and posing a serious threat to the healthy life of the elderly. Sarcopenia has an insidious onset and is often overlooked in clinical treatment. Its pathogenesis is complex, involving functional changes and pathological alterations in multiple systems, presenting significant challenges for related research. Cell models can effectively simulate the pathological changes of diseases under controllable conditions, facilitating the exploration of the etiology and influencing factors of sarcopenia and providing an important approach for in-depth study of its mechanism of action. However, there is currently no standardized cell model in the field of sarcopenia research. Commonly used cell models at present include those involving protein metabolism intervention, oxidative stress, and inflammatory response intervention. This article systematically reviews and discusses the commonly used skeletal muscle cell types and modeling methods, providing a solid foundation and important methodological reference for further simulation of the pathological process of sarcopenia in subsequent experimental studies.
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The Role of Astrocyte-Neuron Energy Metabolism Coupling Imbalance in the Pathogenesis and Progression of Alzheimer's Disease and Research Progress on Traditional Chinese Medicine Interventions

Yang Yuxin, Shao Shitai, Wang Wenpan, Wang Pan, Xie Zhishen, Sun Yiran, Zhang Zhenqiang, Ma Huifen

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Disorders in energy metabolism are a critical factor contributing to cognitive dysfunction. Astrocytes, as key suppliers of energy substrates to neurons, engage in extensive energy metabolism activities in the brain under the coordination of various energy supply mechanisms to sustain normal cognitive function. Imbalances in astrocyte-neuron energy metabolism coupling lead to abnormal neuronal activity, thereby driving the pathogenesis and progression of Alzheimer"s disease (AD). Investigating the pathological mechanisms and therapeutic targets associated with AD from the perspective of energy metabolism is essential for future disease treatment and intervention. Traditional Chinese medicine (TCM), characterized by its multi-component and multi-target effects, has shown potential in regulating cerebral energy metabolism, suggesting that modulating brain energy metabolism may represent a significant pathway for TCM in ameliorating AD. This review systematically elucidates the mechanistic role of astrocyte-neuron bioenergetic coupling dysregulation in the pathogenesis and progression of AD, and critically evaluates recent advancements in therapeutic interventions mediated by TCM.
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Ecological Adaptation Study on Body Weight and Blood Biochemical Parameters in Wild Hainan Macaque Subspecies (Macaca mulatta)

Liu Baozhen, Wang Jun, sun ruiping, Wu Chenfeng, Zhao Xinyuan, Zhao Jianguo, Yuan Jingli

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Objective To compare the body weight , blood physiological, and biochemical indicators of the Hainan macaque subspecies (Macaca mulatta brevicaudata) , and to provide a reference for the subsequent breeding of experimental animals breeding. Methods This study selected 180 wild Hainan subspecies of macaques (both female and male) from the South Bay Macaque Reserve in Lingshui Macaque Nature Reserve as the research subjects. The body weight of the macaques was measured using an electronic scale, and blood samples were collected. Blood routine indicators (RBC, HGB, WBC, PLT, etc.) were detected using an automated blood cell analyzer, and biochemical indicators (ALT, AST, GLU, BUN, etc.) were measured using an automated biochemical analyzer. Data analysis was performed using SPSS software for descriptive statistics, and t-tests were used to compare the differences in body weight and blood indicators between different genders and age groups of macaques. Results The results showed that in adult wild Hainan subspecies of macaques, the body weight of males was significantly higher than that of females (P<0.05). However, there was no significant difference in the results of complete blood cell counts between female and male macaques (P>0.05). In terms of blood biochemical indicators, significant differences were observed in lactate dehydrogenase (LDH) and total bilirubin (TBIL) levels between female and male Hainan subspecies of macaques (P<0.05), while no significant differences were found in other biochemical indicators. Conclusion This study established baseline data on the body weight, blood physiological and biochemical indicators of wild Hainan macaques, providing a reference for the future breeding of Hainan macaques as experimental animals.
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Investigation into the Mechanism of Shanggan Granules in Suppressing the TLR4/NF-κB Signaling Pathway to Alleviate Pulmonary Inflammatory Response in H1N1-Infected Mice

LI Mao, GUO Zhihong, LIU Linjie, ZHANG Mengnan, LI Xiuyuan

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Objective: To explore the mechanism of Shanggan granules on pulmonary inflammation in mice infected with influenza virus. Methods: The model of pulmonary infection with influenza virus was established by nasal inoculation with influenza A/PR8/34 virus. The groups were divided into normal control group, model group, positive control group, low-dose Shanggan granules group, medium-dose Shanggan granules group, and high-dose Shanggan granules group. The treatment lasted for 7 days. After the experiment, the body weight and lung wet weight of the mice were detected. Hematoxylin-eosin staining was used to observe the pathological changes of the lung tissues. The levels of TNF-α, IL-6, IL-8, and TGF-β in the lung tissues were detected by enzyme linked immunosorbent assay. SOD, GSH-Px, and MDA in lung tissues were detected by the kit method. TLR4/NF-κB inflammatory signaling pathways were detected by real-time PCR. Western blot detects the TKB1/IRFs signaling pathway. Results: Compared with the model group, both Shanggan Granules and oseltamivir phosphate reduced the wet weight of the lungs in mice infected with influenza virus, decreased the infiltration of inflammatory cells in lung tissue, reduced the levels of inflammatory factors TNF-α, IL-6, IL-8 and TGF-β, decreased the levels of SOD and GSH-Px in lung tissue, and increased the level of MDA. In addition, mRNA levels of TLR4, MyD88 and p38 and protein expression of TKB1/IRF3/7/NF-κB signaling pathway were inhibited. Conclusion: Shanggan granules could effectively reduce lung injury, lung inflammation, and oxidative stress, and its mechanism might be related to the down-regulation of TLR4/NF-κB inflammatory signaling pathways.
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Exploration of a method for evaluating a rat model of uterine adhesions

cuichuting, Li Junwei, Fang Yi, Zan Yan, Ren He, Xia Liangjun

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Objective To explore the methods of grading the degree of uterine adhesion in the rat model of uterine adhesion. Methods 10 cases of a rat model of uterine adhesion were established by the double injury method. HE staining was used to observe the paraffin sections. Masson staining was used to compare the uterus morphology, the uterine cavity area, and the degree of adhesion. The sections were classified into three grades according to the area of the uterine cavity for comparative analysis. Results The average uterine cavity area and uterine cavity area/endometrial layer area of rats in the model group were smaller than those of rats in the blank group (P < 0.01); the ratio of uterine cavity area/endometrial layer area was categorized into three grades: Ⅰ, Ⅱ, and Ⅲ, and there was a significant difference between the grades (P < 0.05, P < 0.01). Conclusion The uterine cavity area/endometrial layer area of rats with uterine adhesion may reflect the grading difference in the degree of uterine adhesion. It can be used as one of the grading evaluation criteria in the rat model of uterine adhesion, which can provide significance for diagnosing grading in the model of uterine adhesion.
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Effect of macrophage depletion by clodronate liposome on liver tissue transcriptomics in mice with carbon tetrachloride induced liver fibrosis

Wu Hongyu, YANG Zhao, YAN Ruanyu, WANG Shen, SHEN Li, XUE Jingbo, TAO Yanyan, LIU Chenghai, PENG Yuan

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Objective To investigate the characteristics of macrophage depletion by clodronate liposomes (CL) in a carbon tetrachloride (CCl4)-induced liver fibrosis mouse model and analyze transcriptomic features. Methods: Thirty-two C57BL/6 mice were randomly divided into the blank liposome group (CL) and the clodronate liposome group (PL), with 16 mice in each group, receiving intraperitoneal injections of CL or PL. On the 5th day, each group was further divided into control (-N) and model (-M) subgroups, with 8 mice per subgroup. The model group was given 10% CCl4 intraperitoneally to induce liver fibrosis, while the control group received an equal volume of olive oil. After 4 weeks, serum ALT and AST levels were measured; liver inflammation and collagen deposition were observed via HE and Sirius Red staining. RNA was extracted from liver tissues for high-throughput transcriptome sequencing and differential gene expression analysis. Results: Serum ALT and AST levels were significantly elevated in the PL-M group, with fibrosis staging primarily at S3. In the CL-M group, fibrosis staging was primarily at S1. A total of 1,462 and 2,119 differentially expressed genes (|logFC| > 2 and P < 0.05) were identified in the PL and CL groups, respectively. GO analysis revealed enrichment in multiple biological processes, cellular components, and molecular functions in both models. KEGG analysis identified 29 significantly enriched pathways (P < 0.05). RT-qPCR validated the upregulation of genes such as Lgals7 and Timp1 and the downregulation of Mup-ps16 and Mup15, consistent with transcriptomic trends (P < 0.05). Conclusion: This study highlights the characteristics and transcriptomic features of macrophage depletion in the CCl4-induced liver fibrosis model, providing a theoretical reference for research on the immune mechanisms of liver fibrosis.
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Mechanism of CTRP3 regulating SeVGMT to reprogram cardiac fibroblasts into induced cardiomyocyte-like cells

Song Yanbin, Zhang Yunqing, Liu Huiyu, Chen Junming

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Objective　To reveal the efficiency and mechanism of C1q tumor necrosis factor-related protein 3 (CTRP3) regulating Sendai virus (SeV) vector overexpression of Gata4, Mef2c and Tbx5 (SeVGMT) to reprogram cardiac fibroblasts (CFs) into induced cardiomyocyte-like cells (iCMs). Methods　CFs were divided into Control group, NC-Lv group, CTRP3-Lv group, NC-sh group and CTRP3-sh group. NC-Lv, CTRP3-Lv, NC-sh and CTRP3-sh were transfected into CFs using Lipofectamine3000 reagent for 48 h. Then Lipofectamine3000 reagent was mixed with SeVGMT and incubated at room temperature for 48 h. The culture medium was replaced and then cultured for 21 d. The cell morphology at different culture time points (0, 3, 7, 14, 21 d) was observed under a microscope. The expression of myocardial specific proteins α-MHC, α-actin, cTnT, Cx43, Actc1 and Myh6 at different time points were detected by cell immunofluorescence, qRT-PCR and Western blot, and the proportion of beating cells at different time points was calculated. Results　With the extension of culture time, the relative fluorescence intensity, mRNA and protein levels of α-MHC, α-actin, cTnT, Cx43, Actc1 and Myh6 in CFs of each group increased (P<0.05), and the expression levels of the above myocardial specific proteins at 14 d of culture were significantly higher than those at 7 d of culture (P<0.05). At 3 d, 7 d, 14 d and 21 d of culture, the relative fluorescence intensity, mRNA and protein levels of α-MHC, α-actin, cTnT, Cx43, Actc1 and Myh6 in CFs of CTRP3-Lv group increased compared with those of NC-Lv group (P<0.05). Compared with the NC-sh group, the relative fluorescence intensity, mRNA and protein levels of α-MHC, α-actin, cTnT, Cx43, Actc1 and Myh6 in CFs of the CTRP3-sh group were decreased (P<0.05). At 7 d of culture, beating cells appeared in CFs of each group. With the extension of culture time, the proportion of beating cells in CFs of each group increased (P<0.05), and the proportion of beating cells at 14 d of culture was significantly higher than that at 7 d of culture (P<0.05). At 7 d, 14 d and 21 d of culture, compared with the NC-Lv group, the proportion of beating cells in CFs of the CTRP3-Lv group increased (P<0.05). Compared with the NC-sh group, the proportion of beating cells in CFs of the CTRP3-sh group decreased (P<0.05). Conclusion　CTRP3 can enhance SeVGMT reprogramming of CFs into iCMs.
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The protective effect of the novel phosphodiesterase 5 inhibitor CPD1 on promoting autophagy activation in the hearts of rats with pathological myocardial hypertrophy

ZHANG Xue-di, CUI Hua-sui, SONG Ye-ding, Chen Hao-yan, CUI Xi-ping, LI Fang-hong, MU Yun-ping, ZHAO Allan Zi-jian

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Objective To investigate the therapeutic effects of a newly developed PDE5 inhibitor, CPD1, on pathological myocardial hypertrophy induced by abdominal aortic constriction (AAC) in rats, and its impact on the activation of the autophagy signaling pathway in myocardial tissue. Methods Male Sprague-Dawley (SD) rats weighing between 180 and 200 grams were randomly assigned to five groups: control group, the Sham surgery group, AAC model group, the CPD1 treatment group (5 mg/kg), and the sildenafil treatment group (20 mg/kg). The rats underwent blunt dissection of the abdominal aorta at the branch point of the left renal artery beside control group. The AAC model and treatment groups received constriction and ligation surgery, while the Sham group underwent dissection without ligation. After three days of modeling, the treatment group rats received either CPD1 or sildenafil via gavage, while control group, the sham group and model group were administered an equal volume of physiological saline by gavage once daily for eight weeks. Small animal ultra-high-resolution echocardiography and left ventricular catheterization were employed to assess left heart function in rats, calculate the heart mass index, and evaluate the expression of the hypertrophy factor atrial natriuretic peptide (ANP), the key autophagy pathway factor p62, and LC3A/B in rat left heart tissue using Western blot and RT-PCR techniques. Results Abdominal aortic stenosis leads to damage in left heart function in rats, characterized by an increase in cardiac mass index and a significant enlargement of myocardial cell cross-sectional area. The expression of ANP in left heart tissue is significantly elevated (P < 0.05). Additionally, autophagy signaling activity is diminished, with a notable accumulation of LC3-I protein and a reduced conversion to LC3-II. Furthermore, the expression of p62 protein is significantly increased. CPD1 and sildenafil significantly improved left ventricular function in AAC rats, reduced cardiac hypertrophy, inhibited the expression of hypertrophic factors ANP and p62 protein (P < 0.05), activated autophagy signaling, and promoted the conversion of LC3-I to LC3-II. Notably, low-dose CPD1 treatment is equivalent to high-dose sildenafil. Conclusions CPD1 promotes the activation of the autophagy signaling pathway in left heart tissue, inhibits the expression of p62 and ANP, reduces the cross-sectional area of myocardial cells, and improves pathological myocardial hypertrophy as well as left heart function impairment caused by abdominal aortic constriction. Additionally, CPD1 has the advantage of a lower effective dose compared to sildenafil, offering a new option for the treatment of pathological myocardial hypertrophy.
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Calycosin-7-glucoside inhibit lipopolysaccharide -induced neuroinflammation through the TLR4/MyD88/NF-κB signaling pathway

HAN Yu, FENG Yonggang, WANG Mimi, SHAN Kaixin, MIAO Mingsan, FANG Xiaoyan

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Objective To explore the effects and mechanism of Calycosin-7-glucoside (CG) on lipopolysaccharide (LPS) induced inflammatory injury in BV-2 cells and in a mouse model of neuroinflammation. Methods In vitro neuroinflammation model was induced by LPS stimulation of BV-2 cells , BV-2 cells were divided into blank (CON) group, model (LPS) group, dexamethasone (DEX) group, low and high dose of Calycosin-7-glucoside (CG 10 μmol/L, CG 20 μmol/L) group. The viability of BV-2 cells was detected by CCK8 assay. The levels of IL-6 and TNF-α in the supernatant of BV-2 cells were detected by ELISA. Griess method was used to measure the level of NO. In vivo, lipopolysaccharide (LPS) was used to induce neuroinflammation in mice,The mice were randomly divided into blank (CON) group, model (LPS) group, aspirin (ASA) group, low and high dose Calycosin-7-glucoside (CG 5 mg/kg, CG 10 mg/kg) groups. Hematoxylin-eosin (HE) staining was used to observe the pathological changes of hippocampus. ELISA was used to measure the serum levels of IL-6 and TNF-α. Immunofluorescence staining was used to observe the polarization of microglia. The protein expressions of TLR4, MyD88, NF-κB (P65) and p-NF-κB (p-P65) in the cortex were detected by Western blot. Results In vitro experiments showed that CG alone or in combination with LPS in the concentration range of 2.5-160 μmol/L had NO significant toxicity to BV-2 cells compared with CON group(P>0.05). The levels of IL-6, TNF-α and NO in the supernatant of BV-2 cells in the LPS group increased(P<0.01). Compared with LPS group, CG significantly decreased the levels of IL-6, TNF-α and NO in the cell supernatant(P<0.05, P<0.01). In vivo experiments showed that compared with the CON group, the hippocampal neurons in the LPS group were arranged loosely and disorderly, and the nucleus showed nuclear pyknosis.. The levels of IL-6 and TNF-α in serum were increased(P<0.05, P<0.01). The number of Iba1+iNOS+ positive cells was increased(P<0.01), the number of Iba1+CD206+ positive cells was decreased(P<0.01), and the expression of TLR4, MyD88 and p-P65 protein was increased in the cortex(P<0.05). Compared with the LPS group, CG improved the pathological damage of hippocampus and inhibited the serum levels of IL-6 and TNF-α(P<0.01). The number of Iba1+iNOS+ positive cells was decreased(P<0.05), the number of Iba1+CD206+ positive cells was increased(P<0.01), and the expression of TLR4, MyD88 and p-P65 protein was significantly down-regulated in the cortex(P<0.05). Conclusion Calycosin-7-glucoside ameliorates neuroinflammation in mice by suppressing the TLR4/MyD88/NF-κB pathway.
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Exploring the Mechanism of Ursolic Acid in the Treatment of Silicosis Fibrosis Based on Network Pharmacology, Molecular Docking, and Experimental Validation

zhanghuning, zhangwenyue, wenshengpeng, changsirong, guoyi, baorui, sunyue, yanganning, liuzhihong

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【Abstract】Objective To explore the mechanism of ursolic acid against silicosis fibrosis based on network pharmacology, molecular docking and in vitro experiments. Methods The ursolic acid targets were obtained from GeneCards, PubChem and other databases. Disease-related databases (GeneCards, OMIM) were searched for targets related to silicosis fibrosis and epithelial-mesenchymal transition (EMT). The micro-biotech platform was used to screen the intersecting targets, and the protein-protein interaction network was constructed through the String database and Cytoscape to screen the core targets. David database was used for GO and KEGG enrichment analysis. Use AutoDock for molecular docking validation. Validation of key targets by beas-2B cell experiments. Results A total of 179 ursolic acid targets, 8023 and 6809 silicosis fibrosis and EMT-related targets, and 133 intersecting targets were obtained. Nine core targets, including Akt1, STAT3 and MMP9, were screened out, among which MMP9 and Akt1 had the highest connectivity in the PPI network. Molecular docking showed that ursolic acid had strong binding activity with MMP9 (binding energy -8.4 kJ/mol) and Akt1 (binding energy -7.9 kJ/mol). KEGG analysis suggested that the PI3K-Akt signaling pathway was a key regulatory pathway. In vitro experiments showed that ursolic acid significantly inhibited the decrease in cell viability induced by SiO2 (CCK8). Decreased p-Akt expression (Western blot); The expression of the fibrosis marker α-SMA and the interstitial marker Vimentin was down-regulated, while the expression of the epithelial marker E-cadherin (immunofluorescence/Western blot) was up-regulated. Conclusion Ursolic acid may play an anti-silicosis fibrosis role by inhibiting Akt phosphorylation and MMP9 expression and regulating the process of EMT. 【Keywords】ursolic acid; silicosis fibrosis; PI3K/Akt signaling pathway; epithelial-mesenchymal transition; Molecular docking
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Effect of circular RNA circ_0004535 on type 2diabetes mellitus combined with metabolism-related fatty liver disease model mice

Zhou Cai-juan, Li Min, Xu Hu, Chen Bing-ru, Meng Qing, Xiong Wei

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Objective　To explore the influence of hsa_circ_0004535 on type 2 diabetes(T2DM) combined with metabolic-associated fatty liver disease(MAFLD) model mice. Methods　From September 2021 to March 2022. Forty-eight healthy Balb/c mice of SPF grade were selected for modeling and grouping, control group, Each group had 6 mice.Control group: normal feed; T2DM group: diabetes model induced by high glucose diet; T2DM combined MAFLD group: high fat and high glucose feed was given at the same time to induce diabetes combined with fatty liver model; T2DM combined MAFLD + hsa_circ_NC group: after 4 weeks of modeling, 10 nmol/only hsa_circ_NC was injected into the tail vein; T2DM combined MAFLD +hsa_circ_0004535 group: after 4 weeks of modeling, 10nmol/only circ_0004535 was injected into the tail vein; T2DM combined MAFLD+miRNA_NC group: after 4 weeks of modeling, 10nmol/only miRNA blank control was injected into the tail vein; T2DM combined MAFLD+miR- 1827agomir group: after 4 weeks of modeling, 10nmol/only miR-1827agomir was injected into the tail vein; T2DM combined MAFLD+miR-1827antagomir group: after 4 weeks of modeling, 10nmol/only miR-1827antagomir was injected into the tail vein; after the interventions, body weight was measured and recorded weekly. Glucose tolerance and insulin tolerance tests were performed; blood lipids and liver function were measured; liver index and insulin resistance index were calculated; and pathological index tests (HE and oil red O staining, immunohistochemistry, TUNEL staining, Masson staining) were performed to measure the degree of hepatic inflammation, fat deposition and fibrosis. Results (1) The body weight, liver weight, liver index, insulin resistance index and biochemical indexes of the animals in the hsa_circ_0004535 injection group were significantly lower than those in the hsa_circ_NC injection group and the T2DM combined MAFLD group (both P < 0.05). (2) HE staining showed that in the T2DM combined MAFLD+ circ_0004535 group, the steatosis vacuoles were reduced and smaller, and the inflammatory cell infiltration was reduced. The results of oil red staining were consistent with those of HE staining. (3) TUNEL staining showed that TUNEL-positive cells were significantly reduced in the T2DM combined MAFLD+hsa_circ_0004535 group (P < 0.05). (4) Masson staining showed that collagen fiber deposition was significantly reduced in the T2DM combined MAFLD+hsa_circ_0004535 group (P < 0.05).Conclusion　The expression of hsa_circ_0004535 and miRNA-1827 plays an important role in regulating lipid metabolism, insulin sensitivity, inflammatory pathways, hepatocyte apoptosis, and hepatic fibrosis-related pathways in the animal model of T2DM combined with MAFLD.
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The role of Nrf2 in vascular cognitive impairment and the progress of traditional Chinese medicine intervention

ZHAO Yiting, QIN Hewei, Liu Jiandong

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Vascular cognitive impairment (VCI) is a syndrome of cognitive decline attributed to vascular risk factors and cerebrovascular diseases. A range of pathophysiological processes, including inflammation, oxidative stress, cell death, disruption of the blood-brain barrier, and synaptic damage, which are induced by vascular injury, are intricately linked to the development of VCI. Nuclear factor E2-related factor 2 (Nrf2), encoded by the NFE2L2 gene, is a potent transcription factor that plays a critical role in antioxidant defense. Extensive research has demonstrated that Nrf2 mitigates oxidative stress and inflammation by upregulating the expression of antioxidant response elements, thereby reducing the production of reactive oxygen species (ROS). Additionally, Nrf2 modulates programmed cell death, enhances blood-brain barrier integrity, and promotes synaptic plasticity, ultimately delaying the progression of vascular cognitive impairment (VCI). Therefore,this review examines the role of Nrf2 in VCI and highlights recent research on traditional Chinese medicine targeting Nrf2 for the prevention and treatment of VCI, providing novel insights and approaches for managing this condition.
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Role and mechanism of m7G methylation modification in tumor drug resistance

LU Lu, YANG Huiting, LIU Boyang, LI Qian, HUANG Bitang, GAO Shenglan, YANG Chunlong, PAN Qingjun

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N7-Methylguanosine(m7G)modification occurs at the 5'cap of eukaryotic mRNA,as well as specific sites on tRNA and rRNA,and is widely present across various aspects of life.Aberrant m7Gmodification is involved in the dysregulation of gene expression and serves as a biomarker for multiple cancers,holding significant potential for applications in tumor diagnosis and therapy.This review summarizes the biological functions and regulatory mechanisms of m7G modification,as well as its potential clinical applications.It highlights the oncogenic roles of aberrant m7Gmodification and its association with prognosis,with a detailed discussion of the role and molecular mechanisms of abnormal m7G modification in regulating drug resistance in various cancers.
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The role of cannabidiol in drug addiction and research progress

Li Xiong, Ding Jiameng, Yan He, Yang Genmeng, Ma Xiao, Hong Shijun, Zhang Dongxian

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Drug addiction is a serious public health problem worldwide for which there are no established therapeutic medications. Since the legalisation of cannabis and the approval of cannabidiol (CBD) by the US Food and Drug Administration, the therapeutic potential of CBD in the treatment of substance abuse has been widely explored. Numerous studies have shown that CBD exhibits therapeutic potential to reduce drug reward in animal models of addiction such as self-administration, conditioned positional preference, and intracranial self-stimulation.CBD can reduce withdrawal symptoms from substances such as amphetamines, opioids, cocaine, marijuana, alcohol, and nicotine.However, the mechanisms by which CBD modulates drug addiction are more complex and are currently understudied. Now, we review the studies related to CBD and addictive drugs with the aim of exploring the regulatory mechanisms of CBD in drug addiction and providing references for the related studies on substance abuse.
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Research progress on maternal obesity leading to offspring myocardial hypertrophy by regulating myocardial metabolism

LI Qi, Jimusi, Nashunbayaer

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The pathogenesis of cardiovascular diseases of individuals is largely resulted from their maternal obesity (MO), which attracts much attention in recent years. In addition to jeopardizing maternal health, MO increases the risks of offspring heart attack via affecting development of cardiovascular system. The prenatal high-calorie intake leads to the fetal overnutrition that alters the use of fatty acids, glucose, and ketones in cardiomyocytes. Studies indicated that the influences of MO on offspring include the cardiomyocyte metabolism and remodeling, as well as heart ROS increase, which therefore stimulates mTOR and Hippo pathways to induce cardiomyocyte proliferation and hypertrophy. Interestingly, Hippo pathway could potentially be a therapeutic target of cardiomyocyte hypertrophy. This review aims to disclose the role of MO in regulating the fetal cardiomyocyte metabolism, the offspring cardiomyocyte hypertrophy and the epigenetic mechanism thereof. Furthermore, the long-term effects of MO on offspring cardiomyocyte health is discussed. It is suggested that the metabolic memory, the cross-generational genetic effects, and the early-life intervention be laid great emphasis for the future researches.
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Research Advances in the Role of NLRP3 Inflammasome in the Pathological Mechanisms of Multiple Sclerosis: A Review

huangsihua, zhouzheyi, wangshuo, zhongjunwei, yanhongen

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Multiple sclerosis (MS), characterized by inflammatory demyelination in the central nervous system, is a complex autoimmune disorder. Prominent symptoms include damage to myelin sheaths in the brain, optic nerve, and spinal cord, as well as axonal dysfunction. The exact causes and mechanisms of MS remain unclear. It is believed that genetic and environmental factors interact through autoimmune mechanisms, potentially triggering the disease. Recent studies suggest that abnormal activation of the NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome may play a critical role in the pathogenesis of MS. In this context, the author reviewed relevant literature from the past decade, summarizing the mechanisms underlying NLRP3 activation and its connection to MS. Based on a comprehensive review of literature published over the past decade, this article systematically analyzes the molecular mechanisms and activation pathways of the NLRP3 inflammasome, as well as its pathological interplay with MS. The findings aim to provide insights into disease progression and potential therapeutic strategies by elucidating the underlying mechanisms involved.
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The rRole of nitric oxide synthase in the pathogenesis of Alzheimer"s disease

Keying Jiang, Ying Liu, Jiaying Liu, Jingyi Li, Zhikui Wu, Yang meiwen, Hong fenfang, Shulong Yang

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Nitric oxide synthase (NOS) and its produced nitric oxide (NO) involve in learning and memory functions. There is increasing evidence that NOS plays an important role in the pathogenesis of Alzheimer's disease (AD) by influencing β-amyloid protein (Aβ) deposition, neuroinflammation, oxidative stress, abnormal microglia activation , damaged synapse , autophagy, abnormal mitochondrial function of nerve cells, and cerebral hypoperfusion or vascular endothelial cell injury. This article summarizes the role of NOS in the pathogenesis of AD in recent years, which will provide new feasible targets for the prevention and treatment of AD.
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Significant Progress in Biomedical Research Accelerated byArtificial Intelligence

LvJianYi, WangChunXi, LiuSiCheng, YeYiLin, ZhangCongRui, LiFeiYang, ZhangZiShan, DuXiaoYan

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【】With the rapid development of biotechnology, researchers are constantly seeking new methods to improve the efficiency and accuracy of biomedical research and drug development, promoting interdisciplinary integration. The rapid advancement of artificial intelligence (AI) technologies has brought unprecedented opportunities to this field. By integrating various AI models, researchers can better utilize multi-omics data, identify disease phenotypes, simulate disease processes, interpret animal behavior, assess treatment effects, improve experimental design, reduce the use of experimental animals, enhance animal facility management, and improve animal welfare.
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Mechanism of action and engineering synergistic strategy of extracellular vesicles in the treatment of premature ovarian insufficiency

shi xuyan, lu jingjing, zhu xiaolan

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Premature ovarian insufficiency (POI) is a clinical syndrome of premature ovarian failure in women of childbearing age, which is characterized by menstrual disorder, fertility decline and perimenopause symptoms before 40 years of age. Recent studies have shown that extracellular vesicles (EVs), as a natural carrier of bioactive molecules, can effectively transport nucleic acids, proteins and other functional substances, and show significant therapeutic potential in improving ovarian tissue damage, promoting granular cell proliferation and inhibiting apoptosis. Although EVs has broad clinical application prospects in the field of regenerative medicine, it still faces technical bottlenecks in the aspects of targeted delivery efficiency, biological stability and large-scale preparation. Innovative modification strategies based on bioengineering technologies - including membrane surface functionalization, precise content loading and microenvironment pretreatment - provide effective solutions to break through existing technical barriers. In this paper, the biological characteristics of EVs and its mechanism of action in the treatment of POI were systematically reviewed, with emphasis on the key technological breakthroughs of engineering modification strategies in improving the therapeutic efficacy of EVs, and the prospects of its future translational application in the field of reproductive medicine were prospected.
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Practice of Operation and Management of Facilities and Equipment in University Experimental Animal Center

Liu Xiong, Pu Zhiliang, Liu Qishuai

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The Experimental Animal Center serves as the most crucial support platform for the development of disciplines such as science, technology, agriculture, medicine, research and teaching in universities, providing a venue for animal experiments for faculty and students. The facilities and equipment of the Experimental Animal Center are the most important safeguards for ensuring the quality of animal housing environments and the health of personnel. This paper summarizes the actual operation and maintenance of facilities and equipment and the management of troubleshooting in Yunnan University Experimental Animal Center in recent three years. This paper deeply analyzes practical experience in daily maintenance, troubleshooting, personnel training, safety management, and operational effectiveness evaluation. The aim is to provide a comprehensive reference for enhancing the stability, reliability, efficiency, and energy conservation of equipment operation in university experimental animal centers, ensuring the safe and efficient operation of these centers.
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Effects of Biejiajian Pill on Malignant Phenotypes and Underlying Mechanisms in Huh7 Cells

Li Yi Heng, XU Junjie, LAN Tao, LI Xin, ZHANG Ronghua, XIONG Yanan, ZHU Lihua, ZHANG Guangling

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【Abstract】 Objective The present study aims to elucidate the effects and mechanisms of Biejiajian Pill (BJJP)-containing medicated serum on the malignant biological behaviors of hepatocellular carcinoma Huh7 cells. Methods CMTM6 (CKLF-like MARVEL transmembrane domain containing 6)-specific siRNA was used to knock down the expression of CMTM6. Normal rat serum and low (0.55 g/kg), medium (1.1 g/kg), and high (2.2 g/kg) BJJP-containing medicated sera were prepared from healthy SD rats. Huh7 cells were cultured with normal fetal bovine serum (BC), normal rat serum (NC) and low, medium and high doses of drug-containing serum of BJJP (LBJJP, MBJJP and HBJJP), respectively. BJJP-containing serum and si-CMTM6 were applied to Huh7 cancer cells, and the cell proliferation, migration and invasion abilities were evaluated by CCK-8 and Transwell asssays, respectively. Western blot was used to detect the protein expression levels of proliferating cell nuclear antigen (PCNA), epithelial mesenchymal transition (EMT) markers (E-cadherin, N-cadherin, Vimentin), and CMTM6. Results CMTM6 knockdown significantly reduced the mRNA and protein expression level of CMTM6 in Huh7 cells (P<0.05). No significant differences were observed between BC and NC groups in proliferation, migration, invasion, or expression levels of PCNA, EMT markers, and CMTM6 (all P>0.05). BJJP-containing serum treatment markedly inhibited Huh7 cell proliferation, migration, and invasion, downregulated PCNA, CMTM6, N-cadherin, and Vimentin expression, while upregulating E-cadherin compared to NC group (all P<0.05). CMTM6 knockdown suppressed malignant behaviors, with reduced PCNA, Vimentin, N-cadherin and elevated E-cadherin expression (all P<0.05). Conclusions BJJP-containing medicated serum significantly inhibits Huh7 cell growth, invasion, migration, and EMT progression, potentially mediated through CMTM6 suppression.
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To Study the Anti-central-fatigue Effect of Maca via Mitochondrial Biogenesis by AMPK/SIRT1/PGC-1 Pathway in Rat

YAO Wenhuan, ZHOU Wen, LI Yaxuan, LI Ziyao, ZHANG Jing, LV Shibo, LI Hui

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Abstract：objective To examine the anti-central-fatigue function of maca and its underlying mechanism . Methods: A central fatigue rat model was established by multi-factor modeling method with cold-water swimming、sleep deprivation、restraining and tail-clamping. 0.6、1.2、2.4g/kg.bw maca were respectively treated to rat by gavage for 35 days. Behavioral testing was studied by morris water maze test, sucrose preference test and tail suspension test. The markers of oxidative stress in hippocampus such as superoxide dismutase (SOD) 、malondialdehyde (MDA) and catalase (CAT) was detected by test kits. The proteins connected with AMPK/SIRT1/PGC1-α signaling pathway in hippocampus were detected by western blot. Results: Compared with modle group,maca significantly decreased the escape latency and quadrant activity time and the tail suspension time and the content of MDA while increased the times of crossing the platform and the sucrose preference and the activities of SOD and CAT. And maca significantly upregulated the expression of the proteins connected with AMPK/SIRT1/PGC1-α signaling pathway in hippocampus. Conclusion: Maca can improve the indicators in central fatigue rats connected with behavioral testing and oxidative stress . The underlying mechanism may be related to its regulatory effect on the the proteins in AMPK/SIRT1/PGC1-α signaling pathway .
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The effects of four different modeling methods on HPA axis, hemorheology, platelet aggregation rate and myocardial ischemia in rats.

LuFangge, LuYaxi, WuGe, YangPing, WangQian, PanYangyu, LuoYanna, WangChengxiang, KongPengyun, YangLiqiang, LiXiiaohong

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Objective? To observe the effects of four different modeling methods on the hypothalamus ?pituitary ?adrenal (HPA) axis, blood rheology, platelet aggregation rate and myocardial ischemia in rats, and to provide new ideas for the establishment of a rat model of “double heart” disease that is more in line with clinical diagnosis and treatment characteristics. Methods ?Sixty-nine male SD rats were randomly divided into the normal group, the chronic unpredictable mild stimulation (CUMS) group, the isoproterenol (ISO) group, the high-fat diet(HF
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The application of mind mapping in the teaching of experimental animal anatomy

YANG Sheng, MA Zhiyu, LIU Qi, ZHANG Jinlong, CHEN Fenglei

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Experimental animal anatomy plays a significant role in experimental zoology, veterinary medicine, and other life sciences. Integrating mind mapping into the entire teaching process can effectively aid teachers in optimizing the organization of teaching contents and stimulate students’ enthusiasm and self-motivation for learning. This manuscript aims to explore the feasibility, advantages, and challenges of applying mind mapping tools in experimental animal anatomy teaching. It analyzes different application scenarios from the perspectives of both teachers and students, aiming to provide practical teaching tools and methodologies for enhancing instructional effectiveness in experimental animal anatomy education.
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Research progress on the pathogenesis and treatment of high altitude heart disease

WANG Shiwei, KANG Longli

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The oxygen division pressure in high-altitude areas is low. If you are exposed to high-altitude areas for a long time, the body will be in a state of low-pressure hypoxia. Low pressure and hypoxia will stimulate a variety of mechanisms in the body, affecting the normal operation of the body. One of the main reactions of the body to hypoxia is hypoxic pulmonary vasoconstriction (HPV). When HPV is aggravated, it will induce altitude heart disease (HAHD). HAHD is a clinical type of chronic mountain sickness (CMS). Its main characteristics are vasoconstriction and hyperproliferative remodeling of the pulmonary artery. The pressure of the pulmonary artery continues to increase, further increasing the posterior load of the right heart and causing right ventricular hypertrophy. It eventually leads to right heart failure or even whole heart failure. Although people in relevant fields have been deeply researching HAHD in recent years, its prevalence rate is still high. Researchers have been committed to finding the ideal treatment for HAHD, but this is a huge challenge. In particular, few people know about the HAHD subtype. The research on the pathogenesis and treatment of HAHD in recent years is reviewed in order to provide new clues for the prevention and treatment of HAHD.
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Research progress of Traditional Chinese Medicine (TCM) in regulating mitochondrial function for treatment of depression

LU Fangying, LI Chao, ZHANG Shangshu, LI Shuhe, WANG Meng

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Depression is a common mental disorder that adversely affects human health and quality of life. Although its pathogenesis remains unclear, a large number of studies in recent years have indicated a close association between depression and mitochondrial dysfunction. This paper explores the mechanism of mitochondrial dysfunction in depression from four aspects: energy metabolism disorders, oxidative stress and inflammatory responses, mitochondrial DNA damage and mutations, and the imbalance of the mitochondrial quality control systems. Additionally, it summarizes recent advances in the use of traditional Chinese medicine (TCM) to treat depression by regulating mitochondrial function. The findings show the potential of TCM in enhancing mitochondrial energy metabolism, reducing oxidative stress and inflammatory responses, improving mitochondrial DNA, and modulating the mitochondrial quality control systems including mitochondrial biogenesis, dynamic function, and autophagy. These insights offer new perspectives for the in-depth study of the pathogenesis of depression and its treatment with TCM.
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Research progress on moxibustion therapy in regulating inflammatory responses for the treatment of bone-related diseases

lixing, Lixiao, Chenxiaoli, Cuilu, Hongxiaojuan, Lixiang

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With the advent of an aging society, bone-related diseases have imposed a substantial burden on both the general population and healthcare systems, highlighting the urgency of finding new treatment methods. The occurrence and progression of such diseases are closely linked to inflammatory responses. Moxibustion, as a traditional external treatment in Traditional Chinese Medicine (TCM), is well-known for its significant anti-inflammatory and analgesic effects. Previous research indicates that moxibustion demonstrates remarkable therapeutic efficacy in treating bone-related diseases. Thus, this paper reviews the impact of moxibustion on inflammatory responses associated with bone-related conditions. The results show that the anti-inflammatory mechanism of moxibustion in treating bone-related diseases involves mediating pro-inflammatory factors, anti-inflammatory factors and related mediators, and regulating signaling pathways (NF-κB、JAK/STAT、MAPK、PD-1/PD-L1、AMPK /ULK1), hypothalamic-pituitary-adrenal axis, regulating the activation of immune cells, autophagy activity, etc. Despite these findings, the anti-inflammatory mechanisms underlying moxibustion treatment for bone-related diseases remain inadequately understood. Future research should focus on utilizing advanced technologies to gain a more comprehensive understanding of the anti-inflammatory mechanisms involved in moxibustion therapy. This approach aims to facilitate better clinical applications and contribute to safeguarding human bone health.
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Toxicological study of macromolecular pharmaceutical excipients on SD rats and Beagle dogs

daijinlong, leixialing, huangyuankeng, guojianmin, chenzhisen, yangwei

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Objective To observe the toxicological changes in Sprague-Dawley (SD) rats and Beagle dogs after continuous administration of the high molecular weight pharmaceutical excipient polyethylene glycol-polylactic acid copolymer (mPEG-PLA), explore possible toxic target organs or tissues and the reversibility of their damage, and provide a reference for evaluating the safety of this high molecular weight pharmaceutical excipient. Methods A total of 120 SD rats and 40 Beagle dogs, half male and half female, were randomly divided into a control group and low, medium, and high dose groups of the test substance. The self-made high molecular weight pharmaceutical excipient was administered by intravenous injection once a day for 90 consecutive days, followed by a 28-day recovery observation period after cessation of medication. The observed indicators included clinical observation, body weight, hematology, blood biochemistry, immune function, and pathological examination, etc. Results Clinical observations mainly showed that Beagles in the medium and high dose groups had swelling or scabs on multiple parts of the body, abdominal swelling, vomiting, reduced activity and diet, etc.; Beagles in the high dose group had increased body weight. Both strains of animals showed a dose-related decrease in peripheral blood monocyte count and percentage, a decrease in total protein and albumin, and an increase in total bilirubin and direct bilirubin; pathological changes related to medication included an increase in the weight of the liver and spleen, and a large number of foamy phagocytic cells were observed in the liver sinusoids, splenic red pulp, and lymph node medulla. In addition, Beagle dogs showed vacuolar changes in the mesangial cells of the glomeruli and proteinuria. Conclusion Under the conditions of this experiment, the high molecular weight pharmaceutical excipient polyethylene glycol-polylactic acid copolymer (mPEG-PLA) can cause defensive reactions such as enhanced phagocytic cell function in the liver, spleen, kidney, and lymph nodes of animals SD rats and Beagle dogs, which can lead to secondary protein loss, edema, and other secondary disease.
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Exploring the effect of schisandra chinensis polysaccharide on mitochondrial autophagy in skeletal muscle of exercise fatigue mice based on Nrf2/ARE pathway

JIANG Junwen, QIN Liwen, SHEN Yangfeng

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Objective To investigate the effect of schisandra chinensis polysaccharide (SCP) on mitochondrial autophagy in skeletal muscle of exercise fatigue mice based on the Nrf2/ARE pathway. Methods A fatigue mouse model was established through swimming training and randomly assigned into a fatigue group, SCP (20 mg/kg) group, Rhodiola (8 mL/kg) group, inhibitor (30 mg/kg ML385) group, SCP+inhibitor group, with normal mice as the control group. Serum was separated and the levels of lactic acid (LA), lactate dehydrogenase (LDH), blood urea nitrogen (BUN) and creatine kinase (CK) were detected.. The liver was isolated, and the levels of malondialdehyde (MDA), hepatic glycogen (HG), and superoxide dismutase (SOD) were detected. Skeletal muscles were isolated, and muscle glycogen (MG), changes of skeletal muscle tissue in exercise fatigue and mitochondrial morphology were detected. The mitochondrial transcription factor A (TFAM), nuclear respiratory factor-1 (NRF-1) mRNA, Nrf2, quinone oxidoreductase 1 (NQO1), heme oxygenase-1 (HO-1), and LC3protein expression were analyzed. Results The levels of HG, MG, SOD, TFAM mRNA, NRF-1 mRNA, Nrf2, NQO1, HO-1, LC3Ⅱ/LC3Ⅰ in fatigue group were lower than those in control group, while the levels of LA, BUN, LDH, CK and MDA were higher than those in control group (P<0.05). The levels of HG, MG, SOD, TFAM mRNA, NRF-1 mRNA, Nrf2, NQO1, HO-1, LC3Ⅱ/LC3Ⅰ in SCP group and Rhodiola Rosea group were higher than those in fatigue group, while the levels of LA, BUN, LDH, CK and MDA were lower than those in fatigue group (P<0.05), The above indexes were opposite in the inhibitor group (P<0.05).. Conclusions SCP promotes mitochondrial autophagy in skeletal muscle of exercise fatigue mice by activating the Nrf2/ARE pathway, effectively exerting anti fatigue effects.
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Effects of electroacupuncture on microglia and inflammatory factors in PCPA-induced insomnia in rats

TAN Tian, ZHANG Meng, LI Cai-qin, TAN Jia-fei, HE Xi, HE Li-juan, HU Bing-qing, GONG Ri-yu, LIU Lian

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Objective To observe the influences of electroacupuncture on the levels of polarization markers and inflammatory factors interleukin 6 (IL-6), interleukin 4 (IL-4), tumour necrosis factor-alpha (TNF-α) and interleukin 10 (IL-10) in rats with para-chlorophenylalanine-induced insomnia (PCPA) and to explore the mechanism of action of electroacupuncture in the treatment of insomnia. Methods Fifty healthy SPF grade SD rats, half male and half female, were collected and randomly divided into 10 in the blank group and 40 in the model reserve group, and in the model reserve group, the insomnia rat model was created by intraperitoneal injection of 500 mg/kg PCPA suspension. 30 rats successfully modeled were divided into model group, electro-acupuncture group, and western medicine(estazolam) group, with 10 rats in each group using the random number table method. The western medicine group was given estazolam 0.2 mg/(kg-d) by gavage; the electroacupuncture group was given electroacupuncture of Shenmen, Sanyinjiao and stimulation of Baihui and Benshen acupoints for 20 minutes each once a day, for 7 consecutive days. After treatment, serum and hypothalamic levels of TNF-α, IL-6, IL-4 and IL-10 were detected by ELISA and Western blot; immunofluorescence staining was used to detect the expression of Iba-1 in hypothalamic microglia and the co-expression of its M1 and M2 subtypes of cellular markers, CD86 and CD163 in rats. Results Compared with the blank group, the sleep latency (SL) of rats in the model group was prolonged (P<0.01), the sleep duration (ST) was shortened (P<0.05), the serum and hypothalamus levels of IL-6 and TNF-α and protein levels of rats in the model group were significantly higher (P<0.01), and the levels of IL-4 and IL-10 were lower (P<0.01); compared with the model group, the electroacupuncture group and estazolam group, SL was significantly shorter (P<0.01), ST was prolonged (P<0.01), the serum and hypothalamus levels of IL-6 and TNF-α and protein levels of rats in the electro-acupuncture group and the estazolam group were significantly lower (P<0.01); IL-4 and IL-10 were higher (P<0.01); compared with the western medicine (estazolam) group, IL-6 content in the electroacupuncture group was even lower (P<0.05). Compared with the blank group, Iba-1/CD86 (M1 type) co-expression was significantly enhanced in the model group (P<0.01), and Iba-1/CD163 (M2 type) co-expression was significantly weakened in the model group (P<0.01). After electroacupuncture and western medicine intervention, Iba-1/CD86 co-expression was significantly weakened in the electro-acupuncture group and estazolam group (P<0.01), and Iba-1/CD163 co-expression was significantly enhanced in the model group (P<0.05). Conclusion Electroacupuncture effectively improved sleep disturbances in rats, and its underlying mechanism may be associated with regulating microglial polarization, downregulating the levels of pro-inflammatory cytokines, upregulating the levels of anti-inflammatory cytokines, and alleviating neuroinflammation, thereby ameliorating sleep.
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Melatonin self-assembling peptide attenuates myocardial ischemia reperfusion injury in mice

wangmeijuan, Lijiao, Liqi, Weiliping

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Abstract Objective To design melatonin (Mel)-based nanomedicines (Mel-NMs) and evaluate their therapeutic effects on myocardial ischemia reperfusion injury in mice. Methods Melatonin self-assembled peptides (Mel-NMs) were synthesized by incorporating the GFFY peptide and a cardiac targeting peptide (CTP), and their structure was characterized using transmission electron microscopy. A myocardial ischemia reperfusion injury model was established in mice by ligating the left anterior descending coronary artery for 30 minutes, followed by reperfusion. Mice were randomly divided into five groups: sham operation, model, Mel, NMs, and Mel-NMs. Treatment was administered intraperitoneally 10 minutes prior to reperfusion, with Mel (5 mg/kg), NMs, or Mel-NMs (containing Mel 5 mg/kg) or an equal volume of solvent for the sham group. Twenty-four hours after reperfusion, cardiac function, apoptosis, and oxidative stress markers were assessed. Results Transmission electron microscopy revealed that Mel-NMs formed worm-like structures. Compared to the sham group, the model group exhibited significantly reduced cardiac function (P < 0.05), increased serum LDH levels, elevated cardiomyocyte apoptosis (P < 0.05), decreased GSH-Px and SOD activities, and increased MDA content (P < 0.05). Treatment with Mel and Mel-NMs significantly improved cardiac function, reduced LDH and MDA levels, and enhanced GSH-Px and SOD activities (P < 0.05), while also decreasing cardiomyocyte apoptosis (P < 0.05). Notably, the Mel-NMs group demonstrated superior outcomes compared to the Mel group in improving cardiac function and reducing oxidative stress and apoptosis levels (P < 0.05). Conclusion Mel-NMs effectively mitigate myocardial oxidative stress and apoptosis, offering a more potent cardioprotective effect than Mel alone.
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Investigation into the underlying mechanism of ozone water intra-articular Injection in modulating miR-214-3p to alleviate cartilage damage in KOA rats via the NF-κB signaling pathway

LIU Min, LI Weiqi, DOU Huiru, ZHOU Youlong

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【】Objective: Investigating the mechanism underlying the effect of intra-articular injection of ozone water on cartilage repair in KOA rats via the miR-214-3p/NF-κB signaling pathway, so as to Provide a theoretical basis for the clinical application of ozone water. Methods: Sixty male SD rats were randomly divided into blank group and experimental group. The experimental group was randomly divided into model group, ozone water treatment group, ozone water + no-load adeno-associated virus (AAV-NC) group and adeno-associated virus group with ozone water + miR-214-3p inhibitor (AAV-miR-214-3p inhibitor). After treatment, the articular cartilage repair status was evaluated by articular cartilage surface gross scoring, HE staining, and modified Mankin"s score; the expression levels of IL-1β, TNF-α, and MMP-13 were detected by ELISA; the protein expression levels of IKKβ, p65, and p-IκBα were detected in cartilage tissues of each group by Western blot ; Real-time PCR (RT-PCR) gene expression of IKKβ, p65, IκBα and miR-214-3p. Results: compared with the blank group, the remaining groups of rats showed different degrees of cartilage damage, and the scores of the ozonated water treatment group and the ozonated water+AAV-NC group were significantly lower compared with those of the ozonated water+AAV-miR-214-3p inhibitor group (P<0.05); ELISA results: the ozonated water treatment group and the ozonated water+AAV-NC group showed significantly lower (P<0.05) scores in IL-1β, TNF-α and MMP-13 contents were significantly lower in the cartilage tissues of rats in the ozonated water treatment group and the ozonated water+AAV-miR-214-3p inhibitor group compared to the model group and the ozonated water+AAV-miR-214-3p inhibitor group (P<0.05); RT-PCR results: in the cartilage tissues of rats in the ozonated water treatment group and the ozonated water+AAV-NC group compared to the model group and the ozonated water+AAV-NC group The mRNA expression levels of IKKβ and p65 were significantly down-regulated, while the mRNA of IκBα was significantly up-regulated (P<0.05).Western blot showed that, compared with the model group and the ozonated water+AAV-miR-214-3p inhibitor group, the rat cartilage tissues in the ozonated water treatment group and the ozonated water+AAV-NC group showed IKKβ, p65 and p-IκBα protein expression levels showed significant down-regulation, on the contrary, IκBα protein expression levels showed up-regulation (P<0.05).Conclusion: Ozone hydrotherapy significantly ameliorated cartilage damage in KOA rats, and its mechanism of action may be related to inhibiting the activation of the NF-κB signalling pathway through up-regulation of miR-214-3p expression and promoting cartilage repair in KOA rats.
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Exploring the mechanism of Jiawei Simiao Powder on monosodium urate crystal-induced RAW264.7 cell inflammation via miR-146a regulation of the TLR4/NF-κB signaling pathway

LI Huayan, SU Peipei, WANG Xin, NIU Yuanyuan, CHEN Zhenheng, SUN Qianhui, DU Mingrui

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Objective: To explore the mechanism by which Jiawei Simiao Powder regulates the TLR4/NF-κB signaling pathway via miR-146a in MSU crystal-induced RAW264.7 macrophage inflammatory models. Methods: A gouty arthritis model was established by inducing RAW264.7 cells with MSU crystals and divided into control, model, Jiawei Simiao Powder, and colchicine groups. Cell viability was assessed using the CCK-8 method. Levels of IL-1β, IL-6, and TNF-α were measured by ELISA. Expression of miR-146a miRNA and mRNA of TLR4, MyD88, TRAF6, and NF-κB p65 was detected by RT-PCR, while protein expression of TLR4, MyD88, TRAF6, and p-NF-κB p65 was evaluated by Western blot. Results: Compared to the control group, the model group showed significantly decreased miR-146a expression (P<0.01) and increased mRNA and protein expression of TLR4, MyD88, and TRAF6, p-NF-κB p65 protein expression, and levels of IL-1β, IL-6, and TNF-α (P<0.01). In contrast, Jiawei Simiao Powder and colchicine groups exhibited significantly increased miR-146a expression (P<0.01) and decreased mRNA and protein expression of TLR4, MyD88, and TRAF6, as well as reduced p-NF-κB p65 protein expression and levels of IL-1β, IL-6, and TNF-α (P<0.01). Conclusion: Jiawei Simiao Powder may alleviate MSU crystal-induced macrophage inflammatory responses by upregulating miR-146a, inhibiting the activation of the TLR4/NF-κB signaling pathway, and reducing the production of inflammatory factors.
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Comparative study on rat models of pulmonary hypertension induced by normobaric hypoxia and hypobaric oxygen.

lihanxue, sunjinlian, zhengdingyu, liuruixin, huayumeiduo, mayan

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Objective To evaluate pulmonary vascular remodeling, right ventricular function, intestinal barrier integrity, and inflammatory factor expression in rat models of pulmonary hypertension (PH) induced by normobaric and hypobaric hypoxia. Additionally, to compare modeling methods and establish an experimental basis for understanding PH pathogenesis and developing treatment strategies. Methods Method: From June to December 2024, eighteen 6-week-old male SPF SD rats were randomly assigned to three groups: normobaric normoxia (Control), normobaric hypoxia (NH), and hypobaric hypoxia (HH). Mean pulmonary artery pressure (mPAP) was measured by right heart catheterization. Right ventricular function was assessed using echocardiography and the right ventricular hypertrophy index. Pulmonary vascular remodeling and intestinal mucosal barrier damage were evaluated via hematoxylin-eosin (HE) staining. Colon permeability was quantified by colon ligation followed by FITC-dextran injection. The expression levels of inflammatory factors in lung and colon tissues were analyzed using enzyme-linked immunosorbent assay (ELISA). Results Right heart function assessment revealed that, compared with group C, rats in groups NH and HH exhibited significantly increased mPAP (P < 0.05), shortened PAAT, and elevated RVHI and RVFWI (P < 0.05). Compared with group HH, rats in group NH demonstrated prolonged PET and a reduced PAAT/PET ratio, indicating more pronounced right heart dysfunction in group NH. Pulmonary vascular morphology analysis demonstrated that, compared with group C, WA% and WT% of pulmonary vessels were significantly higher in groups NH and HH (P < 0.05). Moreover, WA% was markedly increased in group NH relative to group HH (P < 0.05), suggesting more severe pulmonary vascular remodeling in group NH. Intestinal injury evaluation indicated that, compared with group C, rats in groups NH and HH exhibited shortened colon length, mucosal damage, and significantly increased permeability (P < 0.05). Group HH showed more prominent inflammatory cell infiltration compared with group NH, confirming intestinal mucosal barrier damage in both groups. Inflammation assessment of lung and colon tissues revealed that, compared with group C, the expression levels of IL6, IL1β, and IL17a were significantly elevated in lung and colon tissues of rats in groups NH and HH (P < 0.05). Notably, compared with group HH, group NH exhibited significantly higher expression of IL6 and IL1β in lung tissue and IL17a in colon tissue (P < 0.05), while IL6 expression in colon tissue was relatively lower (P < 0.05), indicating local inflammation in lung and colon tissues in both groups. Conclusions Phenotypic differences were identified between the two hypoxia-induced PH rat models, NH and HH, with respect to pulmonary vascular remodeling, right heart function, intestinal mucosal barrier injury, and the expression of inflammatory factors in lung and intestinal tissues. Additionally, our results demonstrate that variations in air pressure significantly contribute to the pathogenesis and progression of PH. Different air pressures may affect the development of PH via distinct mechanisms, thereby offering critical insights for further investigation into the pathological changes of PH, potential therapeutic strategies to mitigate disease progression, and the elucidation of inflammatory mechanisms underlying PH based on the "lung-intestine axis."
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Keywordsgastric cancer ;exosomes ;Angiogenesis;anti-angiogenic therapy

xuxiyao, shiding, shiding, xixiaoxia

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Gastric cancer, as one of the common malignant tumors worldwide, faces many challenges in its treatment, especially in late stage treatment and high recurrence rate. The angiogenesis of gastric cancer is a key process in the growth and metastasis of gastric cancer, therefore, researching and developing anti angiogenesis therapy methods is of great significance for the treatment of gastric cancer. Extracellular vesicles are nanoscale vesicles released by cells, serving as important messengers for intercellular communication. They regulate local and distant cell communication by transporting unique extracellular vesicle components, and can also promote or inhibit the development and progression of gastric cancer by regulating the growth, proliferation, and angiogenesis of tumor cells. Extracellular vesicles transport bioactive molecules from donor cells to recipient cells, leading to reprogramming of target cells and cascade reactions of molecules. In this review, we describe the relationship between extracellular vesicles and tumor angiogenesis in gastric cancer, as well as the current research status of extracellular vesicles in anti angiogenic therapy. Due to the importance of the physiological structure and function of extracellular vesicles in the angiogenesis of gastric cancer, the prospect of combining extracellular vesicles with anti angiogenic therapy for the treatment of gastric cancer is promising.
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The role of copper metabolism in tumor development and tumor immunity

fuliyan, xinqingxuan, yuebaohon

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[Abstract] Copper is an essential trace element that participates in a variety of metabolic and signaling processes in both oxidized and reduced forms.It is closely related to several aspects of tumor development, and changes in copper homeostasis have a significant impact on processes such as tumor cell growth, metastasis, regulation of the tumor microenvironment, oxidative stress, cell signaling, and the escape of tumor cells from immune surveillance.In tumor cells, copper metabolism promotes immune escape from tumors mainly by regulating the expression of programmed death ligand 1 (programmed Death-Ligand 1，PD-L1).Given the important role of copper in tumor immunity, modulating copper metabolism has emerged as a promising therapeutic strategy.This paper reviews the mechanisms of copper regulation in the human body and explores how disturbances in copper metabolism affect tumorigenesis and progression, as well as the immune and tumor microenvironment.The research value of using copper as a target for tumor immunotherapy is also discussed, providing a theoretical basis for future research directions and clinical applications.
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Effects of Tryptophan Hydroxylase 2 Gene Knockout on Adolescent Social Play and Adult Aggressive and Homosexual Behaviors in Male Rats

WU Yao, FAN Pu

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【Abstract】 Objective This study aimed to examine the effects of tryptophan hydroxylase 2 (Tph2) gene knockout on social play behavior during adolescence and aggressive behavior in adulthood in male rats, to examine the role of central serotonin (5-HT) synthesis deficits in social behavior across postnatal developmental stages. Methods Male Tph2 knockout (Tph2KO) and wild-type (WT) rats were used in this study. Locomotor activity and anxiety levels during adolescence were evaluated after 4 weeks of age through the open field test. The adolescent social play behavior was assessed at 5 and 6 weeks of age using the adolescent social interaction test. Locomotor activity and anxiety levels during adulthood were evaluated at 8 weeks of age through the open field test. The adult aggressive behavior was assessed in rats at 10 and 11 weeks of age using the resident-intruder test. Results In the open field test during adolescence, Tph2KO male rats exhibited a significantly shorter total travel distance compared to WT male rats (P < 0.05), while there was no significant difference in central zone exploration time or central zone entries between the two groups (P > 0.05). In the adolescent social interaction test, Tph2KO rats displayed a significant increase in social play behavior (P < 0.05) and a reduction in neutral social behaviors (P < 0.01) compared to WT controls, while there were no significant differences in overall social behaviors (P > 0.05). In the open field test during adulthood, Tph2KO male rats exhibited significantly reduced total travel distance (P < 0.05), a trend toward decreased central zone exploration time (P = 0.1003), and significantly fewer central zone entries (P < 0.05) compared to WT rats. In the resident-intruder test, there were no significant differences in overall social behavior, aggressive behavior, or neutral social behaviors between the two genotypes either (P > 0.05). Notably, Tph2KO rats exhibited increased same-sex mounting behavior during both adolescence and adulthood (P < 0.05, P = 0.076). Conclusion Tryptophan hydroxylase 2 gene knockout significantly increased social play behavior during adolescence and elevated same-sex mounting behavior during both adolescence and adulthood in male rats, while having no significant effect on adult aggressive behavior. These findings suggest that central 5-HT synthesis deficiency exerts a selective modulatory effect on adolescent social behaviors and impacts same-sex mounting behavior across developmental stages.
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Molecular mechanism of action and drug prediction of hepatic sinusoidal endothelial cells regulating hepatic fibrosis through mesenchymal transition

Jiang Ruizhu, Zheng Yang, Wang Lei, Zhang Rongwu, Wang Jiahui, Liao Xilin, Chen Qiong

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OBJECTIVE: To investigate the molecular mechanism of hepatic fibrosis regulation by liver sinusoidal endothelial cells (LSECs) via mesenchymal transition (EnMT) and to predict the natural active components through bioinformatics, machine learning and cellular experiments. METHODS: Hepatic fibrosis (HF) and EnMT gene matrices were obtained, and the intersecting genes were extracted and enriched using Limma difference analysis and WGCNA co-expression network analysis. Combined with Random Forest, SVM-RFE and network topology analysis, the diagnostic genes were screened, and immune infiltration analysis and prediction of natural active ingredients were performed, and finally the expression of diagnostic genes and the pharmacological effects of predicted ingredients were verified by cellular experiments. RESULTS: Differential analysis yielded 3034 EnMT-associated differential genes and 4133 HF-associated differential genes; WGCNA analysis yielded 4589 EnMT-associated Hub genes and 763 HF-associated Hub genes, and 38 intersecting genes were extracted, which were mainly enriched in the pathways of basement membrane and ECM receptor interaction. Four diagnostic genes, CFP, COL4A2, ITGA1 and GRPEL1, were screened by multidimensional analysis. Immune infiltration analysis showed that the diagnostic genes were closely associated with mast cell resting state, memory B cells and memory CD4+ T cells. RT-PCR results showed that the mRNA expression of the four diagnostic genes was significantly increased in the Jagged1-induced model group (P<0.05). The predicted components, sterol, kaempferol and quercetin, all had good binding activities with the diagnostic genes.ELISA experiments further confirmed that all three active components significantly reduced the expression of COL4A2 protein in Jagged1-induced LSECs, with quercetin having the most significant effect (P<0.01). CONCLUSION: In this study, the molecular mechanism of hepatic sinusoidal endothelial cells involved in the pathological process of hepatic fibrosis through mesenchymal transition was elucidated, and a diagnostic marker system with CFP, COL4A2, ITGA1 and GRPEL1 as the core was proposed, and it was found that the natural active ingredients such as quercetin were able to exert anti-hepatic fibrosis pharmacological effects by targeting the diagnostic genes.
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Research Progress on the Modulation of the PI3K/AKT Signaling Pathway in the Treatment of Alzheimer's Disease with Traditional Chinese Medicine

TANG Yuan, LIU Yonglin, ZHANG Wen, SHAO Jian, YANG Lingyu, LI Yiguang, CHEN Jie

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Alzheimer’s disease (AD) is the most common neurodegenerative disorder worldwide, primarily characterized by cognitive impairment and memory dysfunction. Its pathological mechanisms include the toxic deposition of amyloid β-protein (Aβ), neurofibrillary tangles (NFTs) caused by excessive phosphorylation of Tau protein, mitochondrial dysfunction, synaptic impairment, cholinergic system dysfunction, neuroinflammation, and oxidative stress. Current clinical treatments for AD, such as acetylcholinesterase inhibitors and NMDA receptor antagonists, can provide some cognitive benefits but fail to slow disease progression and often cause side effects. Recent studies have shown that traditional Chinese medicine (TCM) can exert therapeutic effects on AD by regulating the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway. This review systematically summarizes research on how TCM, including active compounds, herbal extracts, and formulae, modulates the PI3K/AKT pathway in AD treatment. By integrating recent findings from both domestic and international studies, this paper aims to provide a theoretical foundation for the application of TCM in AD therapy.
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Research progress on the influence mechanism of kynurenine pathway on Alzheimer’s disease

Chen Qini, Ma Yujie, Lai Yaona, Gao Minghuang, Xu Ziqiao, Yang Hongying, Li Weirong, Wang Qi

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Alzheimer "s disease (AD) is a typical progressive neurodegenerative disease,mainly manifested as severe cognitive dysfunction,involving memory, thinking and emotion.Kynurenine pathway (KP) is one of the main metabolic pathways of tryptophan,which is divided into neurotoxicity branch and neuroprotective branch.In recent years,more and more evidence has shown that KP is involved in the pathogenesis of AD.In this paper,the effect of KP on the pathogenesis of AD was analyzed by referring to the relevant literature on KP intervention in AD in PubMed database,which provided an important reference for KP as a target for AD drug development.
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Advances in the pathogenesis of intracranial arterial dolichoectasia induced by matrix metalloproteinases

GUAN Xiaofang, ZHANG Daopei

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Intracranial arterial dolichoectasia (IADE) is a major artery disease characterized by arterial elongation, dilatation and curvature,the pathological mechanism of IADE is not very clear. Recent studies have shown that matrix metalloproteinases (MMPs) are closely related to the pathogenesis of IADE. Therefore, the author summarized the possible pathological mechanism of MMPs induced IADE from four aspects: MMPs activation and IADE occurrence and development, the correlation between MMPs activation and positive remodeling, hemodynamic changes, and the relationship between MMPs activation and IADE, and the relationship between clinical associated diseases with IADE and MMPs,providing more possible therapeutic targets for effective prevention and treatment of IADE.
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Practical Research on Enhancing the Teaching Effectiveness of Animal Surgery Courses through Life Education

Wenhui Li¹, Yuping Zhang¹, Tiantian Chen², Yi Wu²

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The animal surgery course is a crucial component in training medical students. However, certain deficiencies have been identified in teaching practice, such as the high difficulty of interdisciplinary teaching, students’ weak concepts of sterility, poor clinical thinking, insufficient teamwork, shallow emotional investment, and ineffective value guidance. By integrating the characteristics of student learning and utilizing virtual simulation experiments alongside peer role models, an emotional guidance teaching model has been established to enhance the effectiveness of "life education" through strengthened emotional identification and improved value guidance. Research results indicate that this teaching model forms a closed-loop teaching process, aligns with students" cognitive patterns, cultivates students" comprehensive abilities, and enhances teaching effectiveness.
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RNF130 improves myocardial ischemia-reperfusion injury by inhibiting PARP1 ubiquitination

CHENGUO, LIUMINGHENG, WANGJING, SUJIABAO, WEIMIN, SUNHAIJIAN, ZHUXUEXUE, LUQINGBO

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【】? Objective To investigate the effects and underlying mechanisms of RNF130 (Ring Finger Protein 130) in myocardial ischemia-reperfusion injury (MI/RI). Methods? Male C57BL/6J mice were randomly assigned to four groups (n=6): sham-operated (Sham), myocardial ischemia-reperfusion (IR), myocardial ischemia-reperfusion with empty vector plasmid (IR+Vector), and myocardial ischemia-reperfusion with RNF130 overexpression (IR+RNF130 OE). Mice underwent 24 hours of myocardial ischemia-reperfusion, after which cardiac function was assessed using echocardiography. Cardiac tissues and serum were subsequently collected. Histopathological examination was performed using immunohistochemistry (IHC), dihydroethidium (DHE) staining for oxidative stress, and TUNEL staining to evaluate apoptosis. Protein expression levels were analyzed by Western blotting, [①]immunofluorescence, and IHC. Proteomic analysis was conducted to identify downstream targets of RNF130, and protein-protein interactions were assessed via immunoprecipitation (IP). Results? Compared to the control group mice given an empty vector plasmid, the overexpression of RNF130 in mouse cardiac myocytes led to a significant increase in RNF130 protein expression and a marked improvement in cardiac function, as evidenced by increased values of left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS), as well as a significant reduction in the area of myocardial infarction. Additionally, the expression levels of NOX-2 and BAX proteins were observed to decrease significantly. HE staining revealed that the arrangement of myocardial fibers in the RNF130 overexpression group was more orderly compared to the Vector group, with a reduction in the areas of myocardial cell destruction and necrosis, and an improvement in inflammatory cell infiltration. DHE and TUNEL staining indicated that, compared to the Vector group, the rate of myocardial cell oxidative damage and apoptosis in RNF130 overexpression mice was significantly reduced. Proteomic analysis showed that, compared to the RNF130 overexpression group, there were 75 proteins significantly upregulated and 49 proteins significantly downregulated in the model group mice. We selected the top five proteins with the most significant increase in expression for IP experiments and found that protein PARP1 interacted notably with RNF130. Western blot (WB) experiments revealed that, contrary to the expression changes of RNF130 protein, the expression of RNF130 protein was significantly increased in I/R mice compared to Sham mice, and after overexpressing RNF130, the expression of PARP1 protein was further reduced, and the ubiquitination level of PARP1 was significantly enhanced. ?Conclusions? RNF130 overexpression provides a protective effect against ischemia-reperfusion injury, likely by promoting the ubiquitination and degradation of PARP1. This mechanism may mitigate DNA damage and apoptosis in cardiomyocytes, offering potential therapeutic insights for ischemic heart disease.
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The Research Progress of Acupuncture in Promoting Neurological Remodeling After Intracerebral Hemorrhage

dongshanshan, luoenli

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Neural remodeling is the key to neurological recovery after intracerebral hemorrhage (ICH). The early stage of stroke is a sensitive period for brain plasticity, during which the brain initiates complex processes such as neurogenesis, synaptic remodeling, and angiogenesis to promote collateral circulation and achieve structural and functional remodeling. Acupuncture, a critical therapy in traditional Chinese medicine for treating brain disorders, has demonstrated significant efficacy in promoting neurological recovery after ICH in both clinical and experimental studies. However, systematic reviews of the mechanisms by which acupuncture regulates neural remodeling after ICH remain limited. For the first time, this review provides a multi-dimensional summary of the mechanisms by which acupuncture facilitates neural remodeling after ICH, including: (1) promoting neurogenesis and synaptic remodeling, (2) modulating the damaged microenvironment, (3) optimizing neuroelectrophysiology, (4) improving hemodynamics, and (5) facilitating angiogenesis. By systematically summarizing these mechanisms, this review highlights the therapeutic potential of acupuncture and aims to advance its further research and application in the field of neuroscience.
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Research progress on animal model analysis of colorectal cancer

CAI GUO LIN, GAO YOU WEN, GAO HONG BIN, WU YU''E, GUAN YE ZHI

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Colorectal cancer (CRC) is the third most common malignant tumor in the world, given that it ranks third for incidence, after lung cancer and breast cancer. It’s also the second leading cause of cancer-related death. The causes of CRC are complex, treatment options are dependent on the stage of the disease. The purpose of this review is to critically assess the perspectives of pathogenesis and characteristics of clinical indicators from traditional Chinese medicine and Western medicine. Moreover, the updated method and mechanisms of modeling of the existing animal models of CRC are provided. The results are showing that current CRC animal models are almost entirely based on modern medical modeling techniques and the evaluation criteria are also mainly based on Western medicine diagnostic indicators. These models are limited because they are lacking of combining traditional Chinese and Western medicine for disease diagnosis and treatment, making it difficult to elucidate the mechanisms for CRC developing. Besides, reliable large animal models are rarely reported. Therefore, a better understanding of the mechanisms of integrated traditional Chinese medicine and Western medicine for CRC may provide needed insight to improve the predictability of animal models.
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Research progress on mitochondrial dysfunction and the pathogenesis of migraine

nansonghua, pengchaojie, heqiqi, lizhenjia, yule, shizijian, houluyang, cuiyinglin

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Migraine is a common neurological disorder, and its pathogenesis is complex and not fully understood. In recent years, the role of mitochondrial function in the pathogenesis of migraine has attracted widespread attention. This article reviews the latest research progress on the relationship between mitochondrial dysfunction and migraine, including mitochondrial energy metabolism, oxidative stress, calcium homeostasis, and neuroinflammation. The article first introduces the epidemiology and clinical characteristics of migraine, and explores in detail the key role of mitochondria in these processes. Research has found that mitochondrial dysfunction may lead to increased neuronal excitability, abnormal vasoconstriction, and inflammatory responses, thereby inducing migraine. Based on the evidence of mitochondrial involvement in the pathogenesis of migraine, this article summarizes the current research progress on mitochondrial dysfunction and the pathogenesis of migraine, and proposes future research directions and potential treatment strategies, aiming to provide new ideas for the prevention and treatment of migraine.
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The Impact and Clinical Potential of RNA Modifications in the Development and Progression of Renal Cancer

YANG Huiting, LU Lu, LI Qian, LIU Boyang, GAO Shenglan, HUANG Bitang, YANG Chunlong, PAN Qingjun

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Renal cancer is a common and increasingly prevalent malignancy with a complex pathogenesis influenced by genetics, smoking, and obesity. Current treatment mainly involves surgery, with adjunctive chemotherapy, radiation, and immunotherapy, but high recurrence and metastasis rates limit effectiveness, emphasizing the need for better therapeutic targets. Growing evidence indicates that epigenetic modifications, particularly RNA modifications, play a critical role in renal cancer development and progression. This review highlights recent advances in renal cancer epigenetics, focusing on RNA modifications such as N6-methyladenosine (m6A), N7-methylguanosine (m7G), 5-methylcytosine (m5C), N1-methyladenosine (m1A), adenosine-to-inosine (A-to-I), N6,2'-O-dimethyladenosine (m6Am), and N4-acetylcytidine (ac4C), along with their regulatory factors. It also explores the potential of targeting RNA modifications and associated proteins for diagnosis and therapy.
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The Glymphatic System and Parkinson’s Disease: Current Concepts, Mechanisms, and Therapeutic Perspectives

YANG JIE LI, LAN RUI, ZHANG YONG, TANG CHEN

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The glymphatic system is a recently discovered essential waste clearance pathway in the central nervous system that plays a pivotal role in maintaining brain homeostasis. Growing evidence suggests that dysfunction of this system is closely associated with the pathogenesis of various neurodegenerative disorders. However, its precise mechanistic involvement in Parkinson's disease remains incompletely understood. This review systematically summarizes the structural and functional characteristics of the GS, provides an in-depth exploration of its potential role in PD pathophysiology, and synthesizes current research evidence on GS-targeted therapeutic strategies. The aim is to establish a theoretical foundation for advancing the understanding of PD pathogenesis and developing novel diagnostic and therapeutic approaches.
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Exploring the dilation effect of luteolin on rat thoracic aortic rings based on Kv7 ion channels

wangxingru, yangzerong, wuli, dengwenjuan, songhaorui, Chenchaoyang, liweiping

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【Abstract】Objective To investigate the vasodilation effect of luteolin (Lut) on isolated rat thoracic aorta with endothelium denuded (DRTA) vascular rings and whether its mechanism is related to Kv7 channel. Methods The tension of the DRTA vascular rings was measured with an ex vivo tissue perfusion muscle tone detection system. The DRTA vascular rings were pre-contracted with 60 mM KCl or 0.3 uM U46619, and the effect of luteolin on vascular ring relaxation was observed at 1, 3, 10, 30, 100 and 300 uM. And the effect of 4-AP, XE-991 and ML213 on vasodilation of luteolin was observed. The expression of KCNQ1-KCNQ5 in thoracic aorta was detected by Real-time fluorescence quantitative PCR, and the effect of luteolin on the expression of KCNQ1-KCNQ5 was observed. Western blot was used to detect the expression of Kv7.1 and Kv7.4 proteins inDRTA . Results The maximum vasodilation rates of luteolin on 60 mM KCl and 0.3 uM U46619 pre-contracted in DRTAwere (97.67 ± 8.51)% and (98.42 ± 9.76)%, respectively. And the vasodilation effect showed concentration-dependent characteristics (P<0.05). 4-AP (3 mM) could significantly decline the vasodilation effect of luteolin on DRTA vascular rings at 10 uM, 30 uM and 100 uM (P<0.05). And XE-991 (3 uM) could significantly decline the vasodilation effect of luteolin on DRTA vascularrings at 30 uM and 100 uM (P<0.05). ML213 (1uM) can significantly enhance the vasodilation effect of luteolin on DRTA vascular rings at 3 uM, 10 uM, and 30 uM (P<0.05). In the normalDRTA , The gene expression levels of each subtype of Kv7 channel from high to low were KCNQ1 > KCNQ5 > KCNQ4 > KCNQ3 > KCNQ2. KCNQ1 was the most expressed. Luteolin significantly enhanced the expression of KCNQ1 at 3, 10, 30, 100 uM, and increased the expression of KCNQ2 at 1, 3, 10, 30, 100 uM (P<0.05), and enhanced the expression of KCNQ3 at 3, 10, 30, 100 uM, and enhanced the expression KCNQ4 at 10, 30, 100 uM (P<0.05), however, luteolin did not significantly enhance the expression of KCNQ5 at 1, 3, 10, 30, 100 uM (P>0.05). Luteolin significantly increased the expression of Kv7.1 protein at 3, 10, 30, 100 uM (P<0.05), and significantly increased the expression of Kv7.4 protein at 10, 30, 100 uM in DRTA (P<0.05). Conclusion Luteolin can dilateDRTA vascular rings, which can be attenuated by Kv7 nihibitors. And luteolin can promote the expression of Kv7.1 and Kv7.4 proteins. It is suggested that the vasodilation effect of luteolin may be related to the enhancement of Kv7.1 and Kv7.4 protein expression. This effect makes luteolin a potential therapeutic agent for the prevention and improvement of vascular myogenic response disorder or vasospasm of the thoracic aorta.
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Role of autophagy regulators in myocardial hypertrophy

zhangjun, zhouxinyu, wanjuan, zhangxin

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【】Myocardial hypertrophy is characterized by the heart"s deleterious response to various stressors, leading to an increase in the size of cardiomyocytes and subsequent cardiac dysfunction. Autophagy is a catabolic degradation process necessary for maintaining cellular homeostasis, and has become an important mechanism for the development of myocardial hypertrophy in recent years. This review draws on insights from recent molecular, cellular, and pharmacological studies to comprehensively explore the dual role of autophagy compounds in myocardial hypertrophy. We investigated the contribution of autophagy flux in cardiomyocytes under physiological and pathological conditions, highlighting the complex interactions between autophagy and cardiomyocyte growth, survival, and function. In addition, we discuss the potential of modulating autophagic activity through drugs as a treatment for myocardial hypertrophy and heart failure. A critical examination of established models and the exploration of new autophagy regulators bring us closer to elucidating the complex mechanisms that control myocardial hypertrophy and facilitate the development of targeted therapies. Ongoing research in this area is expected to elucidate the definitive role of autophagy regulators, providing insights into their therapeutic potential and implications for clinical interventions in myocardial hypertrophy and related pathologies.
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Research Progress on the Involvement of Striatal Abnormal Temporal and Spatial Development in Repetitive and Stereotyped Behaviors in Autism

zhouzhangying, donganqin, xuhongyan, cuixinxin, hetingli, huwenjing, zhangzhe, hanyanan, chengdanmeng, liliguo, tangyoucai, dongxianwen

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The incidence of autism is rising annually, and the repetitive stereotyped behaviors that characterize its core symptoms are varied and challenging to treat due to unclear pathogenesis. The striatum is an important brain region for behavioral research, with a unique mosaic structure, complex neural origin, and finely regulated developmental process, which is highly susceptible to genetic and environmental influences. Both clinical and basic studies have indicated that abnormal development of the striatal nuclei may contribute to the pathogenesis of these repetitive stereotyped behaviors in autism. Previous clinical imaging data have primarily revealed variations such as the general outline of the nuclei; however, they have been unable to detect the internal microstructure within these nuclei. By examining abnormalities in the spatiotemporal development of the striatum, we aim to advance our understanding of repetitive stereotyped behaviors associated with autism and provide guidance for future animal experiments and clinical research endeavors.
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Mechanisms of ferroptosis regulated by VDAC3 in sepsis-induced myocardial injury

WANG Jiali, ZHOU Huiting, WANG Nana, XIA Xuexia, CAO Yue, ZHANG Fan, HUANG Xin, LI Na, HUANG Jie

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Objective To explore the potential mechanism of ferroptosis regulated by VDAC3 in sepsis-induced myocardial injury. Methods A total of 20 male C57BL/6J mice (7~8 weeks old) were randomly divided into 2 groups, respectively named Sham group and CLP group, with 10 mice in each group. Sepsis was induced by the cecal ligation and puncture (CLP) . The levels of IL-6, TNF-α, CK-MB, and cTnT in the serum were detected by enzyme-linked immunosorbent assay (ELISA); the pathological changes of the heart tissue were observed by hematoxylin and eosin (H&E) staining; the structural and functional changes of the heart were evaluated by echocardiography; the changes of total glutathione , reduced glutathione (GSH), oxidized glutathione (GSSG), and malondialdehyde (MDA) in the heart tissue were detected by spectrophotometry; the morphological structure of mitochondria in mouse cardiomyocytes was observed by transmission electron microscope; the expression levels of IL-6, IL-1β, VDAC3, GPX4, SLC7A11, LCN2 and PTGS2 mRNA were detected by real-time quantitative polymerase chain reaction (qRT-PCR); and the expression levels of VDAC3, GPX4 and SLC7A11 proteins were detected by Western blot. Results The levels of IL-6, TNF-α, CK-MB and cTnT in the CLP group mice were significantly higher than that in the Sham group (P<0.05). After 24 h of CLP, it was observed that myocardial fibers were torn, the ventricular wall was thickened and edematous, and mitochondrial membrane was ruptured, mitochondrial cristae were broken or even disappeared. Moreover, the GSH levels were significantly reduced in the CLP group compared with the Sham group (P<0.05) ; the lipid peroxide MDA were increased in the CLP group(P<0.05). Furthermore, compared with the Sham group, the levels of VDAC3, GPX4 and SLC7A11 mRNA and protein were all lowered (P<0.05) in the CLP group, and the expression levels of IL-6, IL-1β, LCN2 and PTGS2 mRNA were increased (P<0.05). Conclusions VDAC3 expression decreases in myocardial injury, and it may participate in the occurrence of sepsis-induced myocardial injury by regulating ferroptosis.
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Research progress of animal models and related evaluation indexes of laryngeal reflux disease

WEI Xiuhong, ZHEN Zen, ZHANG Junbo, MA Yanmiao, LI Xianyu

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Throat reflux disease (LPRD) is a disease that occurs in both the upper respiratory tract and the upper digestive tract. The pathogenesis is complex and there is still a lack of effective treatment. Reasonable animal models and standard evaluation methods are particularly important to explore the pathogenesis and develop new therapeutic drugs. New Zealand rabbits are commonly used to model the disease, and balloon dilatation is commonly used to model the disease. The standard evaluation methods of this disease include symptom observation and evaluation, imaging evaluation and PH monitoring. The animal models and evaluation indexes of pharyngeal reflux were reviewed in detail by referring to domestic and foreign literatures, in order to provide reference for future research.
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Research progress of epigenetic modification in renal damage caused by hyperhomocysteinemia

jieyuzhen, Ding Ning, Lu Guanjun, Ma Shengchao

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【】Chronic kidney disease (CKD) is a group of clinical syndromes of chronic kidney structure and dysfunction caused by various causes, with high treatment costs and poor prognosis. As an important regulator of gene expression, studies have shown that the effect of epigenetic modification on gene expression and cell function plays a key regulatory role in the occurrence and development of CKD. Homocysteine (Hcy) is a common amino acid-containing thiol group in the body. As an independent predictor of end-stage renal disease morbidity and mortality, HHcy involves many organs and is highly harmful. This article introduces the relationship between HHcy and chronic renal injury, and further reviews the research progress of epigenetic modification in the mechanism of homocysteine-mediated chronic renal injury, aiming to gain a deeper understanding of the occurrence and development of chronic renal disease The process and its mechanism provide some new ideas and theoretical basis for the research of chronic kidney disease.
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The research progress on the pathogenesis and Chinese medicine intervention of osteosarcoma based on signaling pathways

zhoouhaidong, luyaohong, fanshaoyong

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Osteosarcoma (OS) is a common primary malignant tumor of bone tissue, with high mortality, disability, metastasis and recurrence rates. Its pathogenesis is complex, which seriously affects the quality of life of patients and brings a huge economic burden to families and society. Traditional Chinese medicine has the characteristics of "multi-target, multi-component and multi-pathway". In recent years, a large number of animal or cell model experimental studies have found that The mechanism of OS progression is related to Notch, MAPK, Wnt / β-catenin, PI3K/Akt, Hedgehog and nuclear transcription Nf-κb, transforming growth factor-β (TGF-β)/Smad(Smad) and signal transducer and activator of transcription (STAT) pathways are closely related. Traditional Chinese medicine (TCM) can affect the biological processes such as cell proliferation, migration, invasion, apoptosis and autophagy by interfering with the above signaling pathways to play an anti-tumor role. Based on the cell signaling pathway, this study expounds the role of the above signaling pathways in OS, and summarizes the research status of traditional Chinese medicine intervention in the prevention and treatment of OS at home and abroad in recent years, aiming to provide a reference for further research on the treatment of OS with traditional Chinese medicine, in order to provide new ideas for clinical treatment of OS.
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A Review of Animal Models of Alzheimer's Disease Applied in Traditional Chinese Medicine Research

peijinying, liujialin, liubin, dongxiaohong, 任秀敏, congshuyuan

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Alzheimer's disease (AD) is an age-related neurodegenerative disease, which is mainly manifested clinically as progressive cognitive impairment and memory and language function impairment. With the acceleration of the aging process of China's population, the number of people suffering from AD in China is also increasing. The exact pathogenesis of AD is still unclear, and the current treatment strategy is mainly symptomatic treatment. Animal models are important tools for preclinical research, which are used to explore the molecular mechanism, behavioral function and treatment strategy of the disease. In the future, the mechanism research and drug development of AD need to establish animal models that are consistent with clinical pathological characteristics. This article mainly summarizes the AD animal models commonly used in research reports in recent years, and elaborates on the strains, age, modeling methods, modeling doses, research on Chinese medicine components and pharmacodynamic mechanisms of related AD animal models, in order to provide some references for the establishment of new animal models in the future or for in-depth exploration of the specific pharmacological activities, targets, metabolic pathways and clinical applications of each component in Chinese medicine.
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Progress of experimental research on the mechanism of action of cinnamon against central nervous system diseases

FAN Qinghua, ZHOU Keqing, WU Xiaoyan, WU Xuzhou, HU Yueqiang

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Cinnamomum cassia Presl belongs to the camphor family of evergreen tree plants, and its bark is used as medicine. It mainly contains volatile oil, polyphenols, polysaccharides, flavonoids, flavanols and other chemical constituents, which have the effects of inhibiting neuroinflammatory response, oxidative stress, neuronal apoptosis, neuroprotection as well as improving cerebral ?ischemia-reperfusion. With the progress of modern medicine, the drug is found to have unique advantages in the prevention and treatment of central nervous system diseases (CNSD), and cinnamon and its preparations have been widely used in the treatment of neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, so cinnamon treatment of CNSD has become one of the hot research directions. At present, the mechanism of action of cinnamon in the nervous system has not been comprehensively outlined and summarised, therefore, this paper summarises the progress of experimental research on the treatment of CNSD with cinnamon at home and abroad in recent years by summarising the progress of experimental research on the treatment of CNSD, to provide evidence-based medical evidence for the clinical research and development of the use of cinnamon.
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Research progress on intestinal flora and its metabolites in leukemia and its complications_^*

Liu Jie, Zhang Mei-ling, Chen Shu-peng, Wu Zhen-hui, Zeng Ying-jian

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Leukemia is a malignant tumor that originates in the hematopoietic system, and its incidence continues to increase. Recent studies have shown that gut microbiota and its metabolites play an important role in the occurrence and development of leukemia and its complications. The imbalance of intestinal flora may lead to decreased immune function and inflammatory response, becoming one of the key factors promoting the development of leukemia and its complications. It has been found that bacteria such as faecalis and Enterococcus and metabolites such as bile acids, short-chain fatty acids and hydrogen sulfide have a significant impact on the development and prognosis of leukemia, and the use of fecal flora transplantation and probiotics has shown safety and effectiveness in clinical studies of leukemia. In this paper, the role of intestinal flora and its metabolites in the occurrence, development and prognosis of leukemia was reviewed, and the potential of traditional Chinese medicine to regulate intestinal flora and its metabolites in the treatment of leukemia and its complications was discussed.
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Application of Zebrafish in Medical Experimental Zoology Teaching

ZI Hua-xing, DANG Chi, ZHANG Jingjing

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Traditional laboratory animal breeding is costly and time-consuming, which causes certain limitations in the teaching practice of Experimental Zoology. Zebrafish, with its unique biological characteristics, has gradually become a widely used experimental animal model. However, there are still relatively few teaching examples related to zebrafish in Experimental Zoology courses. This paper explores the application of zebrafish by incorporating them into two modules-“Tissue Sectioning Techniques” and “Immunological Techniques”-in the course of "Medical Laboratory Animal Science and Technology." The aim is to utilize their advantages in experimental zoology teaching and explore their potential applications. This study provides a detailed introduction to the experimental procedures, experimental design, and teaching content involving zebrafish, aiming to offer undergraduate students a more efficient, cost-effective, and practically meaningful experimental teaching platform.
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Characteristics and differences of db/db and KK-Ay Mouse as Diabetic Nephropathy Model

chen qunying, zhoubo, liujing, houyan

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Objective To investigate the characteristics and differences of db/db and KK-Ay mice as diabetic nephropathy (DN) model, and to verify them with Irbesartan treatment. Methods 102 db/db and 102 KK-Ay mice at 12 weeks of age were selected and grouped based on urine ACR (ratio of microalbuminuria MAU and CRE) and UCFP (24-hour total urine protein), then they were given Irbesartan (40mg?kg-1), experimental animal drinking water (model group), and other test articles, with 13 mice in each group. Wild type C57BL/6J (WT) was used as normal control group. Clinical observation was performed daily and mice were weighed every week, together with irregular monitoring of ACR and UCFP. At the end of administration, brain, liver, lung and kidneys were dissected and weighed, organ coefficients were calculated (organ weight ×1000/ animal body weight). Blood was collected and serum TP, Alb, BUN, GLU, TG and CHO were detected. The histopathological changes of renal tissue were observed by HE, MASSON and PAS staining. Results A total of 5 KK-Ay died in 8 weeks and 21 db/db died in 6 weeks;ACR increased with age in db/db and KK-Ay groups, but decreased in Irbesartan groups without statistical difference (p>0.05); UCFP increased with age in KK-Ay group and decreased significantly after Irbesartan treatment (p?0.05); Compared with WT, renal coefficients of db/db and KK-Ay mice had no significant changes (p>0.05), liver coefficients increased significantly (p?0.01), head coefficients decreased significantly (p?0.01), but they did not change after Irbesartan treatment (p>0.05); Compared with WT, serum GLU and TG of db/db and KK-Ay mice were significantly increased (p?0.01), but only that of KK-Ay mice were significantly decreased after Irbesartan treatment (p?0.01); Both db/db and KK-Ay kidneys showed an increase in mesangial matrix and mesangial cells proliferation, and the lesion degree was reduced in the Irbesartan treatment groups. Conclusion Both db/db and KK-Ay at 12 weeks of age can be used as DN models. Compared with db/db, KK-Ay mice have smaller individual differences in ACR and MAU, fewer animal deaths after urine collection, and significant improvements in GLU and TG after treatment, making it more suitable for studying the efficacy and mechanism of DN.
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Exploration of the mechanism of clopidogrel in salt-sensitive hypertension rats

MAO Hongya, JIANG Xiaoliang, LIU Xing, YANG Zhiwei

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Objective To examine the role and mechanism of clopidogrel in the development????????? of salt-sensitive hypertension. Methods Two-month-old Dahl salt-sensitive (Dahl SS) rats and their control salt-resistant (SS13BN) rats were randomly divided into six groups and fed for 8 weeks with normal salt (0.4% NaCl, NS), high salt (8% NaCl, HS), or high salt combined with clopidogrel gavage (10 mg/(Kg·d), HS+CLO). Arterial systolic blood pressure was continuously measured by the tail-cuff method over 8 weeks, and mean arterial pressure was measured by carotid cannulation after 8 weeks (56 days). Renal histopathology was observed by hematoxylin and eosin (HE) staining, renal inflammatory cell infiltration was detected by immunohistochemistry, peripheral blood platelet activation and platelet-leukocyte aggregation were analyzed by flow cytometry, and renal inflammation-related proteins TNF-α, IL-1β, IL-6, and key proteins in the p38MAPK/NF-κB signaling pathway were detected by immunoblotting. Results Compared with the NS group, Dahl SS rats HS group exhibited significantly increased blood pressure, aggravated renal tissue damage, increased inflammatory cell infiltration and expression of inflammatory cytokines, elevated peripheral blood platelet activation and platelet-leukocyte aggregation, and increased expression of p38MAPK/NF-κB signaling pathway proteins. Clopidogrel effectively alleviated these phenotypes induced by high salt in Dahl SS rats. Conclusions Clopidogrel alleviated high salt-induced salt-sensitive hypertension, and decreased? renal inflammatory responses and dysfunction in Dahl SS rats by inhibiting platelet activation and the p38MAPK/NF-κB signaling pathway.
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GDF-15 promotes collateral circulation and improves cardiac function in rats with acute myocardial infarction by activating NO-cGMP-PKG signaling pathway

shang xiaosen, Yang yichun, Hou jianan, Fan linhua, Wei bingyan, Chen zhaoyang

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Objective to observe the effects of growth differentiation factor-15 (GDF-15) on collateral circulation and cardiac function in rats with acute myocardial infarction (AMI) by activating the nitric oxide (NO)-cyclic guanosine monophosphate (cGMP)-protein kinase G (PKG) signaling pathway. Methods The AMI rat model was constructed by ligating the left anterior descending coronary artery. After successful modeling, the rats were randomly divided into sham operation group, model group, and GDF-15 group, with 12 rats in each group. The rats in the GDF-15 group were intraperitoneally injected with recombinant GDF-15 protein, and the other two groups were injected with the same amount of normal saline twice a week for 8 consecutive weeks. Echocardiography was used to detect the cardiac function of rats; HE staining was used to observe the pathological damage of rat myocardial tissue; CD31 immunohistochemical staining was used to observe the collateral circulation in rats; qPCR was used to detect the expression of vascular endothelial growth factor (VEGF) mRNA; kits were used to detect the expression levels of NO, reactive oxygen species (ROS), and cGMP; Western blot was used to detect the expressions of VEGF, eNOS monomer, pser1177eNOS monomer, eNOS dimer, and PKG protein. Results Compared with the sham operation group, the left ventricular end-systolic diameter (LVEDs), left ventricular end-diastolic diameter (LVEDd) increased, the left ventricular ejection fraction (LVEF), and the short-axis shortening rate (FS) decreased in the model group, the myocardial cell necrosis was severe, the vascular density in the infarcted area decreased, the VEGF mRNA level decreased, the levels of NO, eNOS dimer, cGMP, and the expression of PKG protein decreased, and the expression levels of ROS, eNOS monomer, and pser1177eNOS monomer increased (P < 0.05). Compared with the model group, the LVEDs and LVEDd decreased, the LVEF and FS increased, the myocardial cell necrosis was relieved, the vascular density in the infarcted area increased significantly, the VEGF mRNA level increased, the levels of VEGF, NO, eNOS dimer, cGMP, and the expression of PKG protein increased, and the expression levels of ROS, eNOS monomer, and pser1177eNOS monomer decreased in the GDF-15 group (P < 0.05). Conclusion GDF-15 can promote collateral circulation in ischemic myocardium and improve cardiac function by inhibiting eNOS decoupling and activating the NO-cGMP-PKG pathway.
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Comparison of three methods to construct a mouse model of decreased ovarian reserve

linhuadan, wangxu, chenchunhong, weiyuzhuo, luoyanchun, pangfanghui, qinqiuyun, ruanziyun

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Objective To compare the effects on the establishment of the mouse model of diminished ovarian reserve (DOR) by tripterygium wilfordii polyglycosides, cyclophosphamide and cisplatin. Methods Mice were randomly divided into blank group, tripterygium wilfordii polyglycosides (TWP) group, cyclophosphamide (CTX) group and cisplatin (DDP) group. Mice in TWP group were treated with 50 mg/kg tripterygium glycoside suspension by gavage for 14 days, mice in CTX group were treated with 20 mg/kg cyclophosphamide suspension by intraperitoneal injection for 14 days, and mice in DDP group were intraperitoneally injected with 1.5 mg/kg cisplatin solution for 14 days. The body weight, uterine index and ovarian index of mice were recorded; the estrous cycle of mice was observed by vaginal smear method; the levels of anti-Mullerian hormone (AMH), estradiol (E2), follicle stimulating hormone (FSH) and luteinizing hormone (LH) were detected by ELISA; HE was used to detect ovarian follicle development; The maturation rate of oocytes and fertility of mice were analyzed. Results The body weight and ovarian index of the three groups of mice were significantly decreased (P < 0.05); the estrous cycle appeared disorder, with the level of AMH and E2 was significantly decreased (P < 0.05); the rate of developing follicles was decreased, and the rate of atretic follicles was increased (P < 0.05); the maturation rate of oocytes, the pregnancy and live birth were significantly decreased (P < 0.05). Conclusions The DOR mice models were successfully constructed by tripterygium glycosides, cyclophosphamide and cisplatin. the body weight and ovarian index were decreased, the estrous cycle and hormone appeared disorder, and the ovarian reserve function were decreased, resulted in the reduction rate of oocyte maturation, pregnancy and total number of live births; the effect of diminished ovarian reserve was more appropriate in the cyclophosphamide group.
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M2 Macrophage-Derived Exosomes Promote Neural Regeneration by Enhancing the Proliferation of Schwann Cells via the AKT-WEE1 Pathway

wu li mao

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Abstract Background: Macrophages (Mφ) play a significant role in peripheral nerve regeneration. The objective of this study was to investigate the mechanism of action of macrophage-derived exosomes (Exo) in peripheral nerve injury (PNI). Methods The extraction of exosomes (Exo) following the polarization of macrophages (M?) to either the M1 or M2 phenotype. This was done with the intention of intervening in Schwann cells (SCs), and the ensuing experiments included those utilizing the Cell Counting Kit-8 (CCK8), quantitative real-time polymerase chain reaction (qRT-PCR), flow cytometry, sequencing, and Western blot (WB) techniques. In vivo, the sciatic nerve extrusion model was established and divided into PBS, M1-exo and M2-exo groups, which were injected with phosphate-buffered saline (PBS), M1-exo and M2-exo, respectively, while another normal group was set up. The sciatic nerve function index (SFI), wet weight ratio, and musculo-neural tissue staining were evaluated on a weekly basis in each experimental group following surgical intervention. Results M1-exo facilitated SC migration and upregulated glial-derived nerve growth factor (GDNF), whereas M2-exo promoted SC proliferation and migration and upregulated brain-derived nerve growth factor (BDNF) and nerve growth factor receptor (NGFR). Additionally, the following biomarkers were identified: growth factor (NGF), myelin protein zero (MPZ), glial fibrillary acidic protein (GFAP), nerve growth factor receptor (NGFR), and S100 calcium-binding protein B (S100), among others. In vivo, the SFI, wet weight rate, Masson staining of muscle and nerve tissues, and fluorescence area of nerve axons (marker NF200) and SCs (marker S100) in the M2-exo group at week 4 exhibited superior outcomes compared to those in the PBS group, with all differences being statistically significant. Conversely, no significant differences were observed between the M1-exo group and the PBS group. Additionally, both in vivo and ex vivo experiments demonstrated that M2-exo could facilitate the proliferation of SCs through the phosphorylation of serine/threonine kinase (AKT), which subsequently resulted in the downregulation of cell cycle protein WEE1. Conclusion M2-exo enhances the release of nerve regeneration-related genes from SCs, and it can also promote SCs proliferation and migration, thereby facilitating enhanced nerve regeneration through the AKT-WEE1 pathway. Keywords Macrophage (M?); Exosome (Exo); Schwann cells (SCs); Peripheral nerve injury (PNI); WEE1 Chinese Library Classification Number: R651.3
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A Study on the Developmental Toxicity of Dangmu Extract Syrup in 4-day-old SD Rats

daijinlong, guojianmin, chenzhisen, yangwei

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Objective To systematically investigate the impact of Dangmu extract syrup on the growth and development of 4-day-old (PND4) Sprague-Dawley (SD) rats and its toxicological reactions. Methods PND2 pups were randomly divided into a negative control group and low, medium, and high dose groups according to the whole litter design. Starting from PND4, the animals were orally administered with pure water or Dangmu extract syrup once daily for 18 consecutive days, followed by a 15-day recovery observation period after cessation of medication. During this period, the general condition, growth and development, neurological reflex function, spontaneous behavioral activity, hematology, coagulation, blood biochemistry, immune function, growth hormone, and histopathology of the animals in each dose group were assessed. Results At the end of the medication period (PND22), spleen weight and visceral system number of animals in all dose groups were increased compared with negative control group. Histopathological examination showed that spleen nodules did not form in the negative control group, and spleen nodules of animals in all dose groups were formed, larger in volume and more in number than those in the control group, and the degree of change was dose-dependent. After 15 days of recovery after administration, spleen weight of animals in all groups increased with growth and development compared with animals in the same group after administration, and the histopathological examination showed that the spleen structure of animals in all groups was more complete than that after administration, and the spleen nodule structure was obvious, but there was no significant difference between groups. The above changes were related to the development of animal organ structure accelerated by the nutrients contained in the syrup, and had no toxicological significance. No significant abnormal changes were found in other test results. Conclusion The splenic structure of 4-day-old SD rats can be improved in advance with no obvious toxic target organs. In clinical study, attention should be paid to controlling the dosage of the syrups, and regular monitoring of spleen and related blood and blood biochemical indexes should be carried out.
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EV71 induced skeletal muscle injury in BALB/c lactating mice through the Caspase-1/IL-1β signaling pathway

niuhonglin, yangmu, zouxinhong, CaoLin, chenyufei, shiguoxin, liulei, wangbaixin, cuiguoli

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【】 Objective To observe the effect of EV71-induced skeletal muscle injury and to explore the mechanism of Caspase-1/IL-1β signaling pathway in EV71-induced skeletal muscle injury. Methods The 1-day-old BALB/c suckling mice were randomly divided into three groups: normal group (60 pigs), EV71 model group (60 pigs), and cysteinyl aspartate specific proteinase (Caspase)-1 inhibitor (VX765) group (15 pigs). The normal group and the model group were randomly divided into 4 subgroups: 5, 7, 10 and 14d, with 15 animals in each subgroup. 25*103 μl/kg of EV71 virus solution was intraperitoneally injected into one-day-old BALB/c suckling mice for 3 consecutive days. Caspase-1 inhibitor VX765 (20 mg/kg) was injected intraperitoneally 6 hours after virus inoculation, and inoculated daily until the sample was collected. After successful modeling, the body weight and disease scores of BALB/c suckling mice in each group were recorded, hematoxylin-eosin staining (HE) was used to observe the pathological damage of skeletal muscle, and Western blotting and immunofluorescence (IF) were used to detect EV71 VP-1 (EV71 virus-specific capsid protein), pro-caspase-1, Expression of cleaved-caspase-1, IL-1β, a-SMA, and Collegen I proteins. Results Compared with the normal group at the same time point, the EV71 model group had a reduced body weight and increased disease scores. HE staining of skeletal muscle tissue in suckling mice in the EV71 model group showed a large infiltration of inflammatory cells, muscle fascicle rupture and lysis, and a decrease in the cross-sectional area of muscle tissue. Western blot results showed that the levels of EV71 VP-1, IL-1β, a-SMA and Collegen I in the homogenate of skeletal muscle tissue at 5d, 7d and 10d in the EV71 model group were significantly increased (P<0.05). Compared with the EV71 model group, the body weight and clinical disease score of the VX765 group were increased (P<0.05), and the results of Western blot and immunofluorescence showed that Caspase-1 inhibitor could significantly reduce the expression of EV71 VP-1 protein in the homogenate of skeletal muscle tissue of the EV71 model group, and down-regulate pro-caspase-1, cleaved-caspase-1, IL-1β and Collegen I protein level (P<0.05), inhibition of caspase-1 attenuated the effect of EV71 virus on skeletal muscle injury in BALB/c suckling mice. Conclusion EV71 may induce skeletal muscle injury by activating the Caspase-1/IL-1 signaling pathway.
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Network Pharmacology Analysis of Efficacy and Mechanism of Astragalus in the Treatment of Viral Pancreatitis

CAO Xingxin, DUAN Suqin, HOU Jinghan, MA Junchi, LI Aiyi, HE Zhanlong

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Objective This study aims to explore the efficacy and underlying mechanism of Astragalus in the treatment of Viral Pancreatitis using network pharmacology, and subsequently confirm the efficacy and mechanism in cell experiments. Methods Astragalus and Viral Pancreatitis targets were obtained in TCMSP and Gene Cards database, then combining the two results to obtain intersection targets. GO functional enrichment analysis and KEGG signaling pathway enrichment analysis of therapeutic targets were conducted based on DAVID database. The interaction between the therapeutic targets was analyzed by STRING database and Cytoscape 3.10.2, and the core therapeutic targets were screened. PyMOL 3.0 and AutoDock Tolls 1.5.7 were used to complete the molecular docking between the most effective therapeutic components and the core targets. The CVB3 virus was used to construct a viral pancreatitis cell model, and the above core targets were verified. Results 78 therapeutic targets were obtained. The results of enrichment analysis showed that the possible signaling pathways were cancer pathway, lipid and atherosclerosis, PI3K-AKT signaling pathway, etc. In addition, AKT1, TP53, HIF1 A, CASP3, IL-6, MMP9 may be the core targets. The results of cell experiments showed that the expression level of AMY in the model group was significantly increased. The expression levels of AMY, AKT1, TP53, HIF1 A, CASP3, IL-6 and MMP9 in the Astragalus Injection group were significantly decreased compared with the model group. Conclusion Astragalus injection can effectively treat viral pancreatitis, and may play a therapeutic role by reducing the expression levels of AKT1, TP53, HIF1 A, CASP3, IL-6 and MMP9.
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Mechanism of Astragaloside IV in Regulating M2 Macrophage Polarization via the HIF-1α Signaling Pathway in Diabetic Nephropathy

Su Yi, Song Ke

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Objective This study aims to investigate the regulatory effects of astragaloside IV on the HIF-1α signaling pathway in diabetic nephropathy and explore its potential therapeutic mechanisms. Methods: The model of diabetes nephropathy was established by injecting streptozotocin, qRT-PCR and Western blotting were used to assess the effects of astragaloside IV on the expression of Collagen I, α-SMA. Differential gene enrichment analysis was performed on the datasets of diabetic kidney disease patients downloaded from the GEO database, and activated pathways were screened out. Meanwhile, immunohistochemistry and flow cytometry were used to evaluate the effects of Astragaloside IV in reducing renal fibrosis, inflammatory response, and regulating macrophage polarization. Finally, the key role of the HIF-1α pathway in DN was further validated using the HIF-1α inhibitor LW6. Results: The results showed that the GEO database showed that HIF-1 α/NF-κB signaling pathway was activated in patients with diabetes nephropathy. The results showed that astragaloside IV treatment significantly inhibited the expression of HIF-1α and its downstream fibrosis-related molecules in the diabetic nephropathy mouse model, reducing renal fibrosis and inflammatory responses. Astragaloside IV also promoted M2 macrophage polarization while suppressing M1 macrophage activation. The critical role of the HIF-1α pathway in the pathology of DN was further confirmed through experiments using the HIF-1α inhibitor LW6. Conclusion: This study demonstrates that astragaloside IV significantly mitigates fibrosis and inflammation in diabetic nephropathy by regulating the HIF-1α signaling pathway and promotes favorable macrophage polarization.
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Research progress in animal models of IV/SPN coinfection

yang jian shu, wangxuefeng

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Bacterial reinfection in the lungs of influenza patients is a key factor leading to serious illness and death. The adverse consequences caused by co infection of influenza virus (IV) and Streptococcus pneumoniae (SPN) impose a serious burden on patients, and the specific pathogenesis is complex. It is of great significance to better utilize the IV/SPN co infection mouse animal model for later basic research. This article provides a literature review on the reasonable establishment of IV/SPN co infection models under different research backgrounds, providing reference for the selection of animal models in the future.
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The Role and Mechanism of Osteoblast Autophagy in Improving Osteoporosis by Exercise

YI Xiaoyan, ZENG Xinyu, LIU Yuwei, YANG Yuxin, ZHONG Chenghao, HU Jianbo, CHEN Xianghe

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Autophagy of osteoblasts (OB) regulating bone metabolism is a research hotspot in the field of life medicine. OB autophagy can regulate osteoporosis (OP) induced by aging, oxidative stress, estrogen deficiency and glucocorticoid (GCs) treatment by mediating RUBCN, SIRT1, OPG, etc. At the same time, OB autophagy can also regulate OP by activating Notch and FoxOs proteins, up-regulating the expression of osteogenic transcription factors (such as Runx2, Osterix) and mediating AMPK, mTOR, Wnt and JNK pathways to act on OB and osteoclast differentiation. Exercise is an important means to improve OP, and its molecular mechanism is closely related to the up-regulation of PI3K, AMP, TNF-α and SIRT1 expression by exercise. The above factors can activate key factors or pathways such as AMPK, mTOR, Wnt, PI3K/Akt/mTOR, and NF-κB, regulate the expression of downstream target genes (β-catenin, mTOR, FoxO3a, and Bcl-2) to up-regulate the expression of autophagy factors Beclin-1, ATG, and LC3, promote OB autophagy to restore dynamic balance in the body, thereby regulating bone formation and bone resorption, and improving OP. However, the current relationship between exercise, OB autophagy and OP has not been clarified, and there is a lack of systematic review analysis. Therefore, this article intends to review and analyze the mechanism of OB autophagy in the improvement of OP by exercise, and provide a new theoretical basis and research ideas for the prevention and treatment of OP.
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Progress in the study of the relationship between polycystic ovary syndrome and ovarian follicle expansion and its regulatory mechanism

ZHANG Yibo, YANG Li, FENG Shiguang, SUN Jie, HAO Xiaoqiong

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Ovarian follicle expansion is an important part of follicular growth and development into a dominant follicle, which is regulated by a variety of molecules and signals, including follicular cavity formation, follicular fluid accumulation and granulosa cells proliferation. Polycystic ovary syndrome (PCOS) is the most common reproductive endocrine disease in women, and patients mainly present with increased preantral follicles and ovarian polycystic lesions caused by inadequate ovarian follicle expansion. This article summarizes recent new developments concerning the physiological process of ovarian follicle expansion, related regulatory factors and mechanisms, and describes the possible factors of restricted ovarian follicle expansion in patients with PCOS, with a view to providing a theoretical basis for follicular dysplasia, ovulation disorders and other diseases caused by abnormal ovarian follicle expansion.
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A novel anatomical model of the lumbar sympathetic nerve for intrathecal-related studies via a dorsal approach

Gu yinghua, Liu xin, Li yan, Liu wenxun, Ma weiyi, Ye qingshan

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【Abstract】Objective The study attempted to establish a less invasive model for dissecting and monitoring the sympathetic nerve in rats via a dorsal approach for subarachnoid block-related studies. Methods A traditional abdominal approach model and a new dorsal approach model were established in SD rats, and the modeling time of the two models was observed. The stability of the new model was evaluated by measuring blood pressure (BP), heart rate (HR), percentage change in lumbar sympathetic nerve activity (LSNA change %), norepinephrine (NE), and nitric oxide (NO) content after subarachnoid injection of bupivacaine.Results 1.Building a New Model: The time required to create new models for the dorsal approach group (DA group) was shorter than that for the traditional abdominal approach group (VA group), as shown by the results (p < 0.0001).2. Evaluation of the New Model: Compared with the control group, the MAP and SBP were lower at T2 (5 min after injection of bupivacaine into the subarachnoid space) and T3 (10 min ) (p < 0.05); the LSNA change % was significantly different (p < 0.05); the concentration of NE was lower at T3 (p < 0.05). Conclusions The study presents a novel lumbar sympathetic anatomy model using the dorsal approach for subarachnoid-related investigations, which was effectively employed to examine the impact of subarachnoid block anesthesia on lumbar sympathetic nerve activity.
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The expression changes and selection of different internal control proteins in acute hypoxia-induced lung injury by acute high-altitude

Liu jia, Zhang xiaoyu, Zhang yiman, Wang fei, Lai baochang, Zhang jun, Wuren tana, Zheng xiaohui, Tian hongyan, Yin qian

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Purpose The changes of protein expression are involved in the pathophysiological process of acute high-altitude hypoxia-induced lung injury, which is mainly evaluated by western blot. There is no systematic study on the changes of internal control proteins as calibration loading amounts. Methods The low-pressure and low-oxygen chamber was used in the study to induce lunginjury at the altitude of 6000 meters for 8h、24h and 72h. Using HE staining to to confirm the establishment of the lung injury model. Western blot was used to detect the expression of different internal control proteins, including vinculin, α-tubulin, EIF5, β-actin, and GAPDH. At the same time, the total protein expression was detected by Coomassie Blue staining. Further, the bronchial epithelial cells (BEAS-2B) injury model and human umbilical vein endothelial cells (HUVECs) were induced by hypoxia 8h and 24h. And TUNEL staining was used to confirm the establishment of the cell injury model. Western blot was used to detect the expression of internal control proteins as same as that in – vitro model. The total protein expression was detected by Coomassie Blue staining. Results Acute hypoxic models of 8h, 24h, and 72h were successfully established in lung tissue, demonstrating consistent total protein expression and stable levels of internal reference proteins vinculin, α-tubulin, EIF5, and β-actin. The expression of GAPDH was elevated in the 8h, 24h, and 72h groups compared to the control group without statistical significance at 8 h and 24 h but significantly increased at 72h. Similarly, hypoxic models of 8h, 24h, and 48h were successfully established in BEAS-2B and HUVECs with consistent total protein expression. In BEAS-2B cells, the internal reference proteins β-actin and GAPDH exhibited consistent expression with the normoxic control group while vinculin, α-tubulin, and EIF5 showed significantly reduced expression at hypoxic conditions for a duration of up to 24h. In HUVECs, vinculin, α-tubulin and β-actin also maintained consistent expression with the normoxic control group while EIF5 and GAPDH showed significant reduction at the hypoxic time point of 8h and increased expression at 48h. Conclusion Acute hypoxic exposure induces lung tissue injury, and the proteins expression of internal reference proteins vinculin, α-tubulin, EIF5，and β-actin is stable, making the propriate choices for internal references in Western blotting. Additionally, differential protein expression levels for internal reference proteins vinculin, α-tubulin, EIF5, β-actin and GAPDH were observed in BEAS-2B and HUVEC cells when applying Western blotting to the most important lung tissue models invitro, BEAS -2B and HUVECs, to induce hypoxia-induced injury.
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Mechanism of miR-518a-5p/HDAC6 axis in involving in DNA oxidative damage in ovarian cancer SKOV3 cells

Zhu Ling, Cai Weili, Liu Chao, Xu Guoying, Zhang Miao

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Objective To investigate the mechanism of miR-518a-5p/histone deacetylase 6 (HDAC6) axis in involving in DNA oxidative damage in ovarian cancer (OC) SKOV3 cells. Methods The expression of miR-518a-5p and HDAC6 mRNA in OC tissues and different cancer cells (A2780, SKOV3, CAOV3) was detected by real-time fluorescence quantitative PCR (qRT-PCR). SKOV3 cells were separated into Control group, miR-NC group, miR-518a-5p mimics group, miR-518a-5p mimics+pcDNA-NC group, and miR-518a-5p mimics+pc-HDAC6 group. Cell proliferation and apoptosis were analyzed by plate cloning and Hoechst33258 staining. Immunofluorescence assay was applied to detect the expression of phosphorylated histone H2AX (γ-H2AX). Flow cytometry analysis of reactive oxygen species (ROS) levels. The expressions of HDAC6, Bcl-2-associated X protein (Bax) and B-cell lymphoma-2 (Bcl-2) were analyzed by Western blot. The regulatory relationship between miR-518a-5p and HDAC6 was analyzed by dual luciferase assay. The effect and mechanism of miR-518a-5p on oxidative damage of DNA in OC cells were studied by xenotransplantation tumor model. Results The expression of miR-518a-5p decreased and the expression of HDAC6 increased in OC tissues and A2780, SKOV3 and CAOV3 cells (P<0.001). The expression of miR-518a-5p was the lowest in SKOV3 cells and the expression of HDAC6 was the highest, so SKOV3 cells were selected for follow-up experiments. Compared with the miR-NC group, the miR-518a-5p expression, apoptosis rate, number of γ-H2AX positive cells, relative fluorescence intensity of ROS, and expression of Bax in miR-518a-5p mimics group increased, the expression of HDAC6 mRNA and protein, expression of Bcl-2, and colony formation number decreased (P<0.001). Compared with the miR-518a-5p mimics+pcDNA-NC group, the expression of HDAC6 mRNA and protein, colony formation number, and expression of Bcl-2 in miR-518a-5p mimics+pc-HDAC6 group increased, the apoptosis rate, number of γ-H2AX positive cells, relative fluorescence intensity of ROS, and expression of Bax decreased (P<0.001). HDAC6 had a targeted regulatory relationship with miR-518a-5p. The results of in vivo experiments showed that overexpression of miR-518a-5p decreased tumor volume, weight and HDAC6 protein expression in tumor tissue, and increased positive expression of γ-H2AX (P<0.001). After upregulating HDAC6 expression on the basis of overexpression of miR-518a-5p, graft tumor volume, weight and HDAC6 protein expression were increased, while γ-H2AX positive expression was decreased (P<0.05). Conclusion MiR-518a-5p expression is reduced and HDAC6 expression is increased in OC tissues and cells. Overexpression of miR-518a-5p can induce DNA oxidative damage in SKOV3 cells by inhibiting HDAC6 expression, thereby inhibiting cell proliferation and promoting cell apoptosis.
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The Effects of Fuling Xingren Gancao Decoction on DGAT2-Mediated Lipid Metabolism and Vulnerable Atherosclerotic Plaques

Yan Jingjing, Wu Hong

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Objective: To investigate the mechanism by which Fuling Xingren Gancao Decoction stabilizes vulnerable atherosclerotic plaques.Methods: A mouse model of atherosclerosis and a smooth muscle cell lipid accumulation model were established. Histopathological changes in mouse tissues were examined using HE, Sirius Red, and immunofluorescence staining. Lipid deposition in mice and cells was assessed using Oil Red O staining. The expression levels of ABCA1, ABCG1 mRNA, and DGAT2 in mice and cells were measured by real-time PCR and Western Blotting.Results: Animal experiments demonstrated that Fuling Xingren Gancao Decoction increased the content of α-SMA and collagen in plaques, reduced the levels of MMP2 and DGAT2, and decreased lipid deposition. Cell experiments revealed that Fuling Xingren Gancao Decoction lowered DGAT2 expression and lipid accumulation, while promoting the expression of ABCA1 and ABCG1.Conclusion: Fuling Xingren Gancao Decoction stabilizes vulnerable atherosclerotic plaques by reducing lipid accumulation through the regulation of DGAT2 expression.
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miR-204-3p affects silica dust-induced epithelial mesenchymal transition in rat silicosis

YuJing, Chenfang, Huwenxuan, Piyangyang, Zhangxi, Wangluning, Zhaoping, Wangfaxuan

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Objective To explore the role of miR-204-3p in silicosis epithelial-mesenchymal transition，and to elucidate the mechanism by which miR-204-3p affects silicosis fibers by regulating silica dust-induced alveolar epithelial mesenchymal transition process in rats.Methods Forty SD rats were randomly divided into four groups: control group, silicosis model group, miR-204-3p control group (miR-204-3p-NC group), and miR-204-3p Activator group. HE staining and Masson staining were used to observe the pathology of the lung tissue damage in rats; real-time fluorescence quantitative PCR (RT-qPCR) was used to detect the relative expression levels of miR-204-3p and EMT marker genes in the lung tissue of rats in each group. Real-time fluorescence quantitative PCR (RT-qPCR) was used to detect the relative expression levels of miR-204-3p and EMT marker genes in the lung tissues of rats in each group, and Western blot was used to detect the protein expression levels of EMT-related markers in the lung tissues of rats in each group.Results Compared with the control group, the alveolar structure was damaged, interstitial fibrosis of lung septa, and mesenchymal marker expression was elevated in the silicosis model group (P<0.05); compared with the miR-204-3p-NC group, the alveolar structure was more complete, the EMT process was alleviated, the fibrosis was improved, and the mesenchymal marker expression was reduced in the miR-204-3p Activator group (P<0.05). Conclusion Free silica dust can induce epithelial mesenchymal transition in rat lung tissues. overexpression of miR-204-3p has an intervening effect on the epithelial mesenchymal transition process of free silica dust-induced rat lungs, which is expected to affect the fibrosis process of silicosis.Conclusion Free silica dust induces epithelial mesenchymal transition in rat lung tissue. Overexpression of miR-204-3p has an intervening effect on the process of epithelial-mesenchymal transition induced by free silica dust in rats, which is expected to affect the process of silicosis fibrosis.
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Abnormal T cell subsets of BTBR T+Itpr3tf autistic mice at different developmental stages

shenchen, caoxia

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Objective: To investigate the expression of T cell subsets in the spleen of BTBR T+Itpr3tf autistic mouse at 4, 8, and 12 weeks of age, and to determine the optimal age for studying the relationship between immune abnormalities and autism in BTBR autistic mice. Methods: It randomly selected 5-6 male BTBR mouse at 4 weeks, 8 weeks, and 12 weeks of age and C57 mouse of the same gender at corresponding ages for the three-box social interaction test, the self-grooming test, and the marble-burying test; Single cell suspensions were prepared from the spleens of mouse at 8 and 12 weeks of age, and flow cytometry was used to detect 8 subsets of T cells (TH1, TH2, TH17, TC1, TC2, TC17, TFH, and Treg). Results: Compared with C57 mouse of the same age,p＜0.05， BTBR mouse at 4 weeks, 8 weeks, and 12 weeks of age showed a decrease in social time（p＜0.0001，p＜0.0001，p＜0.0001）, an increase in grooming time（p=0.004，p=0.0001，p＜0.0001）, and an increase in the number of marbles buried（p=0.001，p＜0.0001） in BTBR mouse at 8 weeks and 12 weeks of age; As well , the expression of TH1（p=0.0001）, TH2p=0.006）, TC1（p=0.026）, TC2（p=0.0001）, and TFH（p=0.001）cells in 8-week-old BTBR mouse were significantly increased, while the expression of Treg（p=0.0001） cells were significantly decreased; The expression of TH1（p=0.002）, TH2（p=0.009）, TH17（p=0.016）, TC1（p=0.001）, TC2（p=0.0001）, TC17（p=0.005）, and TFH （p=0.0001）increased in 12-week-old BTBR mouse, while the expression of Treg （p=0.01）cells decreased. At different age stages, p＜0.05,the ratio of TH1/Treg and TC1/Treg in 8-week-old BTBR mouse were significantly higher than those in 12 week old mouse, while the TC17/Treg ratio decreased. Conclusions: BTBR mouse at different developmental stages exhibit varying degrees of abnormal increase in Teff/Treg ratio; Based on results of behavioral test, it is recommended to use 8-week-old BTBR mice for research on autism and immune abnormalities.
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The bioinformatic analysis of circadian rhythm gene alterations with brain cell type specificity and their impact on aging

hanxue, guxiaoping

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Objective Facing the challenges posed by population aging, the incidence of age-related neurodegenerative diseases continues to rise, yet their pathogenesis remains elusive with limited therapeutic options. This study focuses on aging as the fundamental basis of disease onset, employing bioinformatic approaches to explore cell-type-specific changes in gene expression during brain aging and their impacts, thereby providing further insights into the biological mechanisms of brain aging. Methods We utilized the Seurat package in R software to integrate, quality control, normalize, and statistically analyze single-cell sequencing datasets (GSE169606) from young and old mouse brains. Through cell type annotation and differential gene expression analysis, we identified differentially expressed genes (DEGs) across various cell types. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were used for functional annotation and enrichment analysis, and the interactions between differentially expressed genes were analysed by Protein-Protein Interaction (PPI). Finally, the four algorithms of MCC, MNC, DMNC and Dgree from the cytoHubba plugin was employed to identify the hub genes in each cell. Results A total of 13 cell types were identified through cell annotation. After comparing the aged group with the young group, we focused on in-depth analyses of the differential genes screened from four major cell types—neurons, microglia, astrocytes, and endothelia. GO analysis revealed that the differential genes in neurons, astrocytes, and endothelial cells were significantly enriched in biological pathways related to circadian rhythm. KEGG analysis found that the differential genes in microglia and endothelial cells were enriched in circadian rhythm-related signaling pathways. PPI analysis demonstrated that the biological networks of differential genes in neurons, microglia, and endothelial cells were significantly enriched in circadian rhythm functional clustering modules. Furthermore, by taking the intersection of four algorithms, we identified core genes within these cell types, and in the process, we also discovered specific variations of circadian rhythm genes in microglia, astrocytes, and endothelial. Conclusion This study employed single-cell transcriptomics technology to reveal the differential expression of genes in neurons, microglia, astrocytes, and endothelial during aging. Hub genes in microglia, astrocytes and endothelial were identified, especially the specific changes in circadian rhythm genes across these three cell types. These findings provide a foundation for further exploring the molecular mechanisms of brain aging and developing related intervention strategies.
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4-week high-intensity interval training regulates skeletal muscle UPRmt in CUMS rats to improve depressive like behavior

HAN Yumei, LIANG Jiaren, BAO Chunhui, ZHANG Ziwei, TIAN Junsheng

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Objective: To investigate the mechanism by which 4-week high-intensity interval training (HIIT) regulates skeletal muscle UPRmt and improves mitochondrial function in chronic unpredictable mild stress (CUMS) rats. Method: 8-week-old Sprague Dawley rats were randomly divided into control group (C group), model group (M group), exercise+control group (HC group), and exercise+model group (HM group). The M group and HM group received an 8-week CUMS to establish a depression model, while the HC group and HM group received a 4-week, 5-day HIIT intervention. The exercise regimen consisted of 3-minute high-speed (85-90% Smax) combined with 1-minute low-speed (50-55% Smax) uninterrupted repetitive training (with Smax set as the maximum training speed). The behavioral changes of rats were evaluated in weeks 4 and 8. Tissue samples were taken 24 hours after the last behavioral test, and the ultrastructure of rat skeletal muscle mitochondria was detected by transmission electron microscopy. ATP and ROS content were measured by Elisa, and the protein expression levels of ATF4, ATF5, CHOP, and HSP60 were detected by Western blot. Result: (1) Compared with group C, the body weight, number of crossing grids, number of upright positions, sugar water preference rate, and ATP content of rats in group M were significantly decreased (P<0.01), while the number of damaged mitochondria, ROS content, ATF4, ATF5, CHOP, and HSP60 protein expression were significantly increased (P<0.01); (2) After 4 weeks of HIIT intervention, compared with group C, the ATP content, ATF4, and ATF5 protein expression in HC group rats were significantly increased (P<0.05, P<0.01); compared with group M, the number of crossing grids, number of upright positions, sugar water preference rate, ATP content, and ATF4 protein expression in HM group rats were significantly increased (P<0.01), while the number of damaged mitochondria, ROS content, ATF5, CHOP, and HSP60 protein expression were significantly decreased (P<0.01, P<0.05); (3) After 4 weeks of HIIT intervention, the number of crossing grids and damaged mitochondria in CUMS rats were positively correlated with ATF4 protein expression, ROS content and CHOP protein expression, damaged mitochondrial number, and ATF5 protein expression. Related, with statistical significance (r>0.75,P<0.01；r>0.75,P<0.05); The number of crossing grids was negatively correlated with CHOP and HSP60 protein expression, the number of upright positions was negatively correlated with ATF5 and HSP60 protein expression, and the sugar water preference rate was negatively correlated with CHOP and HSP60 protein expression, with statistical significance (r<0.75, P<0.05). Conclusion: 4-week HIIT intervention can improve mitochondrial dysfunction and alleviate depressive like behavior in CUMS rats by regulating skeletal muscle UPRm.
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Research Progress on the Antioxidant Stress Regulation of Dopaminergic Neurons in Related Neurological Diseases by Baicalin

DING Xue-ying, ZHOU Rong-yi, MA Bing-xiang, ZHANG Yong-ting, XIE Xin-yue, WU Chen-lei, WANG Meng-fei, ZHANG Yu-yan

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Baicalin, the primary active component of the traditional Chinese herb Scutellaria baicalensis, has garnered significant attention due to its remarkable antioxidant and anti-inflammatory properties. Baicalin exhibits a particular affinity for the dopamine (DA) system, maintaining cerebral DA levels by regulating OS-related pathways, suggesting that the DA system may serve as its "intracerebral target system" to exert neuroprotective effects. Nuclear factor erythroid 2-related factor 2 (Nrf2), a central transcription factor regulating redox homeostasis, plays a pivotal role in the anti-OS process mediated by baicalin. This article systematically reviews the pharmacological effects of baicalin, provides an in-depth analysis of the interaction mechanisms between OS and DN, and focuses on the latest research progress in baicalin's treatment of neurological diseases through the Nrf2 signaling pathway against OS. It offers theoretical insights into the pharmacological and molecular mechanisms of baicalin in regulating the DA system through antioxidant stress for the treatment of neurological disorders.
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Construction and Comparative Study of Vaccinia Virus VR-1354 Infection Models in C57BL/6N and BALB/C Mice

WU YUNXIANG, WANG CHAO, LI SHUN, ZHOU XIAOHUI

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【Abstract】Objective: To construct models of C57BL/6N and BALB/C mice infected with vaccinia virus VR-1354 (WR (NIH TC-adapted)), and compare the differences between the C57BL/6N mouse and BALB/C mouse infection models. Methods: According to the conventional method, vaccinia virus VR-1354 was amplified, concentrated and titrated. The median lethal dose (LD50) of vaccinia virus VR-1354 for C57BL/6N mice and BALB/C mice was determined respectively. Mice of the two strains were infected with the LD50 respectively. The lung tissues of the control group and the experimental group mice were taken for HE staining on the 3rd, 7th and 14th days, and the changes in the virus load in the lung tissues were measured at the same time. Results: (1) The titer of the amplified vaccinia virus VR-1354 was 3 × 10? PFU/mL. (2) The LD50 of vaccinia virus VR-1354 for C57BL/6N mice was 2.5 × 103 PFU, and the LD50 for BALB/C mice was 2.8 × 103 PFU. (3) After infecting mice of the two strains with 2.5 × 103 PFU of vaccinia virus VR 1354, the lung tissue lesions of the mice became more serious as the infection time increased, but the symptoms of the mice tended to recover after the seventh day. (4) The virus loads in the lung tissues of the two strains of mice began to increase on the 3rd day, reached the maximum on the 7th day, and then gradually decreased. Conclusion: The infection models of C57BL/6N mice and BALB/C mice infected with vaccinia virus VR-1354 were successfully established. This virus can cause obvious lesions in the mouse lung tissues, including inflammatory cell infiltration and alveolar cavity fluid exudation, etc. There are certain differences in the degree of disease onset and susceptibility between the two strains of mouse infection models. The susceptibility of C57BL/6N mice to this virus is higher than that of BALB/C mice.
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The role of optic atrophy 1-mediated mitochondrial dynamics in the occurrence and development of central nervous system diseases

QIGEGE, DONGXINGANG, LIWEIFENG, liuyan, lihui, renyiqin, zhangsuqing

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Mitochondria are the center of intracellular energy metabolism.Mitochondrial dynamics refers to the dynamic process of mitochondrial fusion and fission, which plays an important role in maintaining mitochondrial homeostasis and central nervous system function.Optic atrophy 1(optic atrophy 1,OPA1) is a key factor involved in mitochondrial dynamics. By regulating the process of mitochondrial fusion and fission, reducing oxidative stress, inhibiting apoptosis and promoting mitochondrial autophagy, optic atrophy 1 maintains the dynamic changes of mitochondrial quantity, structure and biological function. A large number of studies have shown that OPA1-mediated mitochondrial dynamics plays an important role in ischemic stroke, Alzheimer"s disease, Parkinson"s disease, spinal cord injury, multiple sclerosis and other central nervous system diseases. This article mainly reviews the regulatory mechanism of OPA1 on mitochondrial dynamics and the important role of mitochondrial function mediated by mitochondrial function in central nervous system diseases, in order to provide new ideas for clinical treatment.
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Research progress on the mechanism of acute leukemia mediated by ferroptosis

ZHU Dacheng, LIU Yan, WEI Jiaxu

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Ferroptosis is mainly related to iron, lipid and amino acid metabolic pathways, which contribute to the production of reactive oxygen species, mitochondrial damage and finally cell death. Ferroptosis primarily involves iron, lipid, and amino acid-related metabolic pathways that contribute to the production of lipid reactive oxygen species. In recent years, ferroptosis has been recognized as a key regulatory mechanism during tumor development, and it is no exception in acute leukemia. The purpose of this article is to review ferroptosis and its mechanism in the development of acute leukemia, and to explore how ferroptosis affects acute leukemia,which provides new ideas for future research and treatment of leukemia.
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The ameliorative effect of exercise on Alzheimer's disease and mechanisms

Xu Mingsheng, Sun Kaihong

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The pathogenesis of Alzheimer's disease (AD) is one of the key research focuses in the field of life sciences. Exercise serves as an important intervention for ameliorating neurodegenerative diseases., and studies have demonstrated that aerobic exercise, resistance training, and multimodal exercise combinations can significantly improve AD. Analysis reveals that its pathogenesis is closely associated with the regulation of exercise in suppressing inflammatory responses, optimizing the activation states of astrocytes and microglia, promoting hippocampal neurogenesis, and improving blood-brain barrier function.This article reviews the effects and mechanisms of different exercise methods in improving AD and makes prospects, with the aim of providing theoretical and experimental basis for the exercise prevention and treatment of AD.
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The role of TRIM13 in Endoplasmic Reticulum Quality Control and Its Association with Diseases

YANG Shiying, RONG Yuying, DONG Yuehong, JIANG Lina

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The endoplasmic reticulum quality control (ERQC) system, a core mechanism for maintaining cellular homeostasis, primarily mediates the degradation of misfolded proteins in the endoplasmic reticulum (ER) through two pathways: ER-associated degradation (ERAD) and ER autophagy (ER-phagy). Tripartite motif 13 (TRIM13) is a protein located on the ER membrane, which plays a critical role in ERAD by its E3 ubiquitin ligase activity. In addition, TRIM13 also acts as a non-classical ER-phagy receptor to mediate the occurrence of ER-phagy. In recent years, TRIM13 has received extensive attention in the field of ERQC. This article reviews the structure and function of TRIM13, as well as the mechanisms by which TRIM13 contributes to ERQC, and summarizes its abnormal expression and regulatory role in diseases, with the aim of providing new strategies for the treatment of related diseases.
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Research Progress on the Mechanisms of Neuropilin-1 in Atherosclerosis

ZHANG Xinyi, CAI Hongwen

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Atherosclerosis(AS), the primary pathological basis of coronary heart disease, is of significant importance in the prevention and treatment of coronary heart disease. Neuropilin-1 (NRP1), a member of the neuropilin receptor family, is closely associated with various growth factors, including vascular endothelial growth factor (VEGF) and transforming growth factor-β (TGF-β). NRP1 influences the progression of atherosclerosis through its crucial roles in angiogenesis, inflammatory responses, and the sensing of shear stress on the vascular endothelium. Therefore, a thorough exploration of the mechanisms underlying NRP1's role in atherosclerosis and the development of NRP1-targeted therapeutic strategies will provide new insights into the diagnosis and treatment of atherosclerosis.
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Progress in murine models of pulmonary vascular plexiform lesions of pulmonary arterial hypertension

LI Xinyu, REN Zhouxin

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At present, the intervention of progressive pulmonary vascular lesions has become the bottleneck and the focus of the prevention and treatment of clinical pulmonary hypertension. Plexiform lesions in pulmonary arterioles are the typical pathological manifestation of irreversible abnormal pulmonary vascular remodeling and are the criterion for stage IV pulmonary vascular remodeling. At present, the pathophysiology of the lesion is not perfect, and there are no effective clinical intervention measures. Therefore, it is of great significance to establish the corresponding animal models. This paper introduces the new progress of the stereology of plexiform lesions, focuses on the evaluation of these models, and evaluates the characteristics and uses of these models in order to provide reference for the animal experimental study and mechanism of pulmonary hypertension with pulmonary vascular plexiform lesions.
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Construction and evaluation of animal model of Renal fibrosis with Qi deficiency and dampness stasis

GAO Ranran, HAN Cong, LIAN Menghui, LI Wei

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Abstract:Objective To construct and evaluate a mouse model of renal fibrosis syndrome combined with Qi-deficiency and dampness-stasis, and explain the changes of protein and metabolic pathways by multi-omics.Methods 24 C57BL/6j mice were randomly divided into normal group (N), model group (M) and renal fibrosis disease and syndrome combined group (BZ) with 8 mice in each group. The experiment period was 6 weeks. A mouse model of renal fibrosis with Qi deficiency and dampness stasis was established by "CsA + high-fat diet + swimming exhaustion + constant temperature and humidity" . The model was evaluated by measuring the general signs, observing renal function, tongue RGB (red, green, blue) values, hemorheology indexes, blood lipids, inflammation and oxidation indexes.And combined with renal tissue HE, Masson, PAS, oil red O staining, TUNEL apoptosis, and TGF- β immunofluorescence. Renal proteomics combined with serum metabolomics screened out differential proteins and metabolites and performed pathway enrichment analysis. Results The weight of BZ group began to decline at the 3rd week (P < 0.05), and significantly decreased at the 4th week (P < 0.01). At the same time, the amount of eating and drinking water decreased, the hair disordered and gloss decreased, the spirit decreased, the activity decreased, and the stool was thin. Scr, BUN, UACR and NAG in BZ group were higher than N group (P < 0.05 or P < 0.01), the Scr and NAG level was statistically significant compared with M group. The R value of tongue image in BZ group was significantly lower than N group (P < 0.01), and the B value was higher than N group (P < 0.05). The viscosity of whole blood multi-shear rate and HCT in BZ group were higher than those in N and M groups, and PV was higher than those in N group (P < 0.05 or P < 0.01). The levels of TC, LDL-C, CRP, IL-6 and MDA in BZ group were significantly increased compared with N and M groups (P < 0.01), and the activity of SOD was decreased compared with N group (P < 0.05). In BZ group, renal tubule vacuolation, inflammatory cell infiltration, glomerular basement membrane thickening, collagen fiber hyperplasia and lipid accumulation were evident. Renal cell apoptosis and TGF-β deposition were increased in BZ group. There were 299 different proteins in BZ and N groups, 180 of which were up-regulated and 119 down-regulated. There were 323 differential metabolites, of which 205 were up-regulated and 118 down-regulated. Primary bile acid biosynthesis,Taurine and hypotaurine metabolism,Biosynthesis of unsaturated fatty acids are co-enriched by differential proteins and differential metabolites, involving 3 differential proteins and 9 differential metabolites. Among them, Docosapentaenoic acid (22n-3),Eicosapentaenoic acid,Taurine,3-Sulfinoalanine,Taurocholic acid,Acnat1,Hsd17b12,Acnat2 showed high prediction accuracy.Conclusion It is feasible to construct RF animal model of Qi-deficiency and dampness-stasis by "CsA+high-fat diet + exhaustion of swimming + constant temperature and humidity" method. The Biosynthesis of unsaturated fatty acids andTaurine and hypotaurine metabolism may play an important role in RF animal model of Qi-deficiency and dampness-stasis.
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Study on the technical influencing factors of non-surgical embryo transfer in mice

Li Xiaying

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Objective: We observed the effects of different non-surgical embryo transfer devices, number of transfered embryos, embryo stage, and embryos obtained from differernt mouse strain on the efficiency of non-surgical embryo transfer in mice, as well as compared the efficiency of surgical and non-surgical embryo transfer, to establish a stable non-surgical embryo transfer technology system. Methods and Results: Two different non-surgical transfer devices were used for embryo transfer, and the pregnancy rates were（75±0）%、（66.67±14.43）%，and the birth rates were (46.11±6.31)%, (18.89±0.96)% respectively. The embryo number for transferring is 10, 15, and 20, the pregnancy rates were (66.67±11.55)%, (80.00±0)%, (66.67±23.09)%, and the birth rates were (29.33±4.16)%, (38.67±4.81)%, (17±3.46)% respectively. Blastocysts and morulae were transferred non-surgically, and the pregnancy rates were (80.00±0)%, (146.67±11.55)% respectively, with the birth rates (38.67±4.81)%, (10.22±2.77)%. Four strains (C57, ICR, genetically modified mouse A, genetically modified mouse B) were used as donors for non-surgical embryo transfer, and the pregnancy rates were (66.67±11.55)%, (80.00±0)%, (73.33±11.55)%, (80.00±0)%, with the birth rates (26.67±2.67)%, (38.67±4.81)%, (32±3.53)%, (29.34±2.31)%respectively. 15 pseudo-pregnant mice were transplanted surgically, and 15 pseudo-pregnant mice were transplanted non-surgically, and the pregnancy rates were (80.00±0)%, (86.67±11.55)% respectively. The birth rates were(38.67±4.81)%, (36±5.82)% respectively. Conclusions: The efficiency of non-surgical embryo transfer using the A transfer device was higher on our platform. The embryo transfer efficiency was higher when 15 embryos were transfered into unilateral uterine horns of pseudo-pregnant 2.5-day recipients. The efficiency of blastocyst-stage embryos transfer was higher than morula. There was no significant difference in the efficiency of surgical embryo transfer and non-surgical embryo transfer.
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Zhang Ying1, Xie Lulu2, Zhang Zhaopeng3, Gao Rui1, Wei Xuyang1, Guo Junpeng4?*(1. College of Integrative Chinese and Western Medicine, Changchun University of Chinese Medicine, Changchun, 130117, China.

zhangying, xielulu, zhangzhaopeng, gaorui, weixuyang, jinmeiying, guojunpeng

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【】Objective To investigate the protective effect and mechanism of Polygonatum sibiricum Polysaccharides (PSP) on Diabetic cardiomyopathies (DCM). Methods Forty SPF-grade male SD rats were randomly divided into normal group, model group, PSP group and metformin group. After four weeks of high-fat feeding, streptozotocin (STZ) was intraperitoneally injected to establish diabetes mellitus animal model, and the drug was administered by gavage for 12 weeks, and the body weights and blood glucose were recorded every fortnight. At the 16th week, cardiac function was detected by non-invasive echocardiography; myocardial histopathological changes and the degree of myocardial fibrosis were assessed by HE and Masson staining; serum interleukin-6 (interleukin-6,IL-6), interleukin-1β (interleukin-1β,IL-1β), Interleukin-18 (IL-18), tumour necrosis factor-α (TNF-α), triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL), and high-density lipoprotein (HDL) were detected by enzyme-linked immunosorbent assay (ELISA); The expression levels of fibrosis-related proteins TGF-β1, Smad2, Collagen-Ⅰ, Collagen-Ⅲ and pyroptosis-related proteins NLRP3, ASC and Caspase-1 were detected in rat myocardial tissues by protein immunoblotting (Western blot). Cellular experiments were performed by exposing H9c2 cells to high glucose (40 mmol/L) to mimic the in vitro DCM model, and cell viability was detected by CCK-8 assay; apoptotic cell ratio was detected by flow cytometry. Results Compared with the model group, rats in the treatment group had significantly lower blood glucose, lipid, and serum inflammatory factor levels (P < 0.05), significantly higher Ejection fraction(EF% )and fractional shortening(FS%) values (P < 0.05), and improved cardiac function; myocardial fibers were better aligned, and collagen fiber accumulation was reduced; and myocardial tissues of NLRP3, ASC, Caspase-1, Collagen-Ⅰ, Collagen-III, TGF-β1 and Smad2 protein expression levels were significantly reduced (P < 0.05). In the cellular assay the PSP treatment group increased the viability and decreased the proportion of apoptotic cells in high glucose-induced H9c2 cardiomyocytes. Conclusion PSP can improve glucose-lipid metabolism, protect cardiac function, and delay the occurrence of myocardial fibrosis in diabetic rats, and it can also improve the viability of cardiomyocytes, and its mechanism of action may be related to the inhibition of cellular pyroptosis and delay the occurrence of ventricular remodeling.
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Research on the Relationship between HIF-1α and Cardiac Energy Metabolism

wang xin, Zhai Ziwei, Wang Zhiyang, Zhu Liang, Wu Yunhong

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The heart, serving as the "energy factory" of the human body, is tasked with the critical mission of maintaining blood circulation and oxygen supply,Therefore, its normal functioning relies on the generation of a substantial amount of ATP to support its mechanical activities.. However, under pathological conditions such as myocardial infarction, coronary artery sclerosis, and pulmonary hypertension, insufficient blood supply leads to a reduction in oxygen supply, subsequently activating a series of compensatory protective mechanisms. ,Hypoxia-inducible factor-1α (HIF-1α), a nuclear transcription factor stably expressed under hypoxic conditions,, has been proven to regulate oxygen transport by promoting angiogenesis and vasodilation, and optimize oxygen utilization by regulating the balance of glucose metabolism and lipid metabolism, participating in the regulation of various cardiac diseases. HIF-1α plays a crucial role in regulating cardiac energy metabolism and oxidative stress. This article systematically summarizes the various mechanisms of action of HIF-1α in reprogramming cardiac energy metabolism, combines the latest research results, deeply explores its potential clinical application value in cardiovascular diseases, and proposes future research in directions and possible treatment strategies. By comprehensively summarizing the mechanism of HIF-1α in ischemic heart disease, this article aims to provide new ideas and therapeutic targets for the prevention and treatment of cardiovascular diseases. [Key words] HIF-1α;hypoxia;lipid metabolism;glycolysis;oxidative stress
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Chrm3 regulates LPS-induced inflammation in peritoneal macrophages of Lbp-/- mice via the MAPK/ERK signaling pathway

chenzhida, fubin, lisidi, liusai, guozhongkun, zhangyue, wangkezhou

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Objective To investigate the role of Chrm3 in regulating LPS-induced inflammation after LBP deletion in peritoneal macrophages of LBP knockout (Lbp-/-) mice. Methods Peritoneal macrophages of WT and Lbp-/- groups were isolated to establish an inflammation model induced by LPS. Chrm3 expression in Lbp-/- mouse peritoneal macrophages was inhibited by 4-damp and siRNA. Chrm3 expression was overexpressed by lentivirus. The inhibitor method were divided into a control group, LPS group, and inhibitior group. For siRNA transfection, cells were also divided into control group, LPS group, si-NC group, and si- Chrm3 group. And overexpress ion method were divided into control group, LPS group, negative control group and overexpression group. Changes in the Chrm3 response to LPS stimulation were verified by Western blot. Other methodologies, such as CCK-8, qPCR, and western blot assays, were used to confirm the effect in cell inflammation and the survival rate by 4-damp、si-Chrm3 and lentivirus. Results Significant elevation in Chrm3 protein expression in Lbp-/- peritoneal macrophages was observed post-LPS stimulation (P＜0.001). whereas no notable change was found in the wildtype. A remarkable increase in the cell survival rate was noted in 4-damp and si-Chrm3 groups (P＜0.05,P＜0.01) and the cell survival rate was reduced in overexpression group(P＜0.01). Furthermore, 4-damp and si-Chrm3 groups exhibited significantly reduced expression of inflammatory factors TNF-α、IL-1β and IL-6(P＜0.01,P＜0.001), and p-ERK(P＜0.01,P＜0.001), which are associated with cell damage and inflammation. In contrast,the expression of inflammatory factors TNF-α、IL-1β and IL-6(P＜0.001), and the phosphorylation of p-ERK protein(P＜0.001)were significantly elevated in the overexpression group. Conclusions Following LPS stimulation, upregulation of Chrm3 and proinflammatory cytokine expression was observed in Lbp-/- peritoneal macrophages. Specific downregulation of Chrm3 expression using 4-damp and si-Chrm3 significantly decreased LPS-induced proinflammatory cytokines in Lbp-/- peritoneal macrophages. The upregulation of Chrm3 using overexpressing lentivirus significantly elevated the levels of related inflammatory factors. Chrm3 is implicated in the regulation of the LPS-induced inflammation response in peritoneal macrophages of Lbp-/- mice.
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Teaching and Research of Laboratory Animal Science Support the Cultivation of New Quality and Innovative Talents

WANG Rong, ZHAO Sihai, BAI Liang, WANG Weirong, QU Pengxiang, GUO Long, LIU Enqi

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New quality productivity is a strategic engine for promoting high-quality development in the new era. It is an inherent requirement and important focus for enhancing new driving forces and building new national advantages. Innovative talents cultivation and technological innovation are the key points for the development of new quality productivity. Laboratory animal science is a comprehensive interdisciplinary subject that integrates multiple disciplines such as biology, medicine, pharmacy and biomedical engineering. Teaching and research of laboratory animal science not only promote the construction of innovative talent teams by cultivating innovative consciousness, innovative thinking, innovative spirit, and innovative operational abilities, but also vigorously promote the development of cutting-edge technologies and the transformation of disruptive research results in the fields of basic research and clinical translation of biomedicine, providing important guarantees for China's scientific and technological progress and innovative development.
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Study of the effect of CB1R modulation of synaptic plasticity on ASD-like behavior in mice

Yilin Zhang, Du Caiyao, Guo Peiwen, Cheng Zeyu, Gao Ya, Zou Mingyang, Sun Caihong

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【】? Objective? To investigate the regulation of synaptic plasticity by CB1R and its effects on ASD-like behavior. ?Methods ?CB1R knockout (knockout,KO) mice and valproic acid (VPA)-induced ASD model mice (VPA mice) were used as study subjects. Behavioral experiments assessed the effects of CB1R on ASD-like behavior in mice; neuronal structural integrity and dendritic density were detected by passaging MAP2 staining experiments, and Western Blot experiments detected the expression of synapse-associated proteins to assess the effects of CB1R on synaptic plasticity. Results ?Behavioral results showed that VPA mice had significant ASD-like behavior; CB1R-/- mice had a significantly lower ratio of residence time in the central region of the open field, a significant increase in the number of buried beads and self-combing time, a significant decrease in the time spent socialising with unfamiliar mice2 and exploring unfamiliar objects, and a significant increase in the time spent exploring old objects (P <0.05); CB1R+/- mice had a significantly lower ratio of The ratio of dwell time was significantly reduced, and the number of buried beads and self-combing time were significantly increased (P <0.05). The results of synaptic plasticity assay showed that there was significant synaptic plasticity impairment in VPA mice; the hippocampal MAP2-positive neuron densities were significantly reduced in CB1R-/- and CB1R+/- mice, and the expression levels of SYN1 were significantly increased (P <0.05).? Conclusion ?CB1R knockdown causes mice to exhibit significant ASD-like behavior such as anxiety and repetitive stereotyped behavior, social and cognitive impairments, as well as neuronal damage, dendritic dysplasia and disrupted synaptic protein expression, suggesting that CB1R is involved in regulating abnormal synaptic plasticity as a pathological mechanism for the development of ASD-like behavior.
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Erianin alleviates atopic dermatitis by regulating the HMGB 1 / RAGE-RhoA / ROCK 1 signaling pathway

Xu Kexin, Wang Dandan, Jin Hongyu, Du Yue, Li Li, Song Yilan, Yan Guanghai, Li Liangchang

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Objective: To explore the role of Erianin in specific dermatitis (AD) and its regulatory mechanism in HMGB 1 / RAGE-RHOA / ROCK 1-signaling pathway. Methods: DNCB induced BALB/c mice serve as a model for AD. Measure the skin thickness, spleen, and lymph node weight of mice. Methylamine blue and H&E staining were used to detect pathological changes in the back skin and ears of mice. ELISA detects levels of inflammatory factors. Establishment of an in vitro model of Alzheimer"s disease using HaCaT cells stimulated by TNF - α. Use flow cytometry to detect cellular ROS. Immunofluorescence assay was used to detect mtROS. TUNEL method was used to detect cell apoptosis. Use immunoblotting to detect the expression of HMGB1, RAGE, RhoA, and ROCK1 proteins.Results: It inhibited the increase of skin thickness, reduced the weight of spleen and lymph nodes, improved the infiltration of inflammatory cells, and the degranulation of mast cells, and reduced the level of inflammatory factors. In vitro, Erianin reduced the production of cellular ROS, mtROS induced by TNF- α. The protein expression of HMGB 1, RAGE, RhoA and ROCK 1 decreased. Treatment of r-HMGB1-stimulated HaCaT cells with RAGE-specific blocker (TFA) showed no change in HMGB1 expression, and the expression of RAGE, RhoA, and ROCK1 decreased. In the Rho kinase inhibitor (Y-27632) + TNF- α group, except for RAGE, the results were similar to the TFA + TNF- α group. Conclusion: Erianin relieves atopic dermatitis by regulating the HMGB 1 / RAGE-RhoA / ROCK 1 signaling pathway.
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Study on renal injury in rats after entering a low-pressure and low-oxygen environment from the plain into the plateau

Jia Meng, qu zhen ji mu, suo lang de ji, guo yi dan, guo shi kun, wei hua ying, zhou xiao ling, wang rui ji

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【Abstract】Objective To explore the changes in renal function, renal injury biomarkers, and renal pathology in rats over time after entering a simulating low-pressure and low-oxygen environment from the plains to the plateau. Methods 30 male Sprague-Dawley rats were divided into 5 groups randomly, with 6 rats in each group. The control group was placed outside the chamber under normal pressure and oxygen conditions. The experimental groups were placed in a low-pressure and low-oxygen(LPLO) chamber to simulate a plateau environment at 5000m above sea level, living in the chamber for 3 days, 7 days, 14 days, and 28 days respectively. Observe the renal injury biomarkers of each group: serum creatinine (CRE), serum cystatin C (CysC), serum neutrophil gelatinase-associated lipocalin (NGAL), serum kidney injury molecule-1(KIM-1) and serum interleukin-18 (IL-18) levels. HE staining and PAS staining is used to observe the pathological changes of kidney injury. Results Compared with the control group, the levels of NGAL, KIM-1, CysC, and CRE in the experimental group were significantly increased (all P<0.05). The average diameter of glomeruli was significantly reduced in the LPLO 3day group, significantly increased in the LPLO 14day group (both P<0.05). The PTC/tubule was significant decreased. The renal tubular injury score and OM congestion score were significant increased (both P<0.05). Regression analysis showed that PTC/tubule was linearly negatively correlated with the duration of low-pressure and low-oxygen, while CRE, CysC, and pathological indicators (mean glomerular diameter, OM congestion score, and renal tubular injury score) were curvilinearly correlated with the duration of low-pressure and low-oxygen (all P<0.05). For the variables that showed curvilinear correlation, restricted cubic splines (RCS) analysis was used: each curve exhibited an "inverted L" shape, with inflection points occurring on the 7th day, indicating that the rate of increase for all indicators was highest within the first 7 days of low-pressure and low-oxygen, and the rate of increase slowed from 7 days to 28 days. Conclusions After simulating entering the plateau environment from the plain, there were significant damage in the kidney in terms of structure and function, and the kidney had a self-adaptive adjustment process toward the plateau environment.
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Study on mechanism of Liangxue Tuizi Formula in the treatment of Henoch-Sch?nlein purpura rats through ROS-mediated activation of NLRP3 inflammasome

SONG Jin-wan, REN Xin-qing, XING Qiong-qiong, LI Yi-fan, YANG Man-xiang

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Objective To study the effect of Liangxue Tuizi Formula(LXTZF) on reactive oxygen species(ROS)-mediated NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome activation in Henoch-Sch?nlein purpura rats, and to explore the possible mechanism of Liangxue Tuizi Formula in the treatment of HSP. Methods 24 rats were randomly divided into 4 groups: blank group, model group, LXTZF group and Compound Glycyrrhizin (CG) group. Except the blank group, the rat model of a Henoch-Sch?nlein purpura was established by heat drug combined with egg albumin (OVA). After successful modeling, LXTZF group was given LXTZF solution 7.47 g·kg-1, CG group was given CG solution 13.5 mg·kg-1 by gavage, blank group and model group were given normal saline solution gavage once a day for 4 weeks. Samples were collected 8 hours after the last gavage. Hematoxylin-eosin staining (HE) was used to observe the skin histopathologic changes. Serum Interleukin-18 (IL-18) and Interleukin-1β (IL-1β) levels were detected by enzyme-linked immunosorbent assay (ELISA). The changes of ROS levels in the skin of rats were detected by immunofluorescence. Real-time quantitative PCR (RT-qPCR), immunohistochemical and western blot methods were used to detect Apoptosis-associated speckle-like protein (ASC), NLRP3, Cysteinyl Aspartate-Specific Protease-1 (Caspase-1) gene mRNA and protein expression in rat skin. Results Compared with the blank group, the skin pathology of the model group showed obvious inflammatory cell infiltration. Serum IL-18 and IL-1β levels were significantly increased (P<0.05), skin ROS levels were significantly increased (P<0.05), and skin ASC, NLRP3, Caspase-1 mRNA and protein expression levels were significantly increased (P<0.05). Compared with the model group, the infiltration of inflammatory cells in the skin tissues of rats in the LXTZF group and the CG group was alleviated, the levels of serum IL-18 and IL-1β in the CG group and LXTZF group were significantly decreased (P<0.05). The level of ROS in the skin was significantly decreased (P<0.05), and the mRNA and protein expression levels of ASC, NLRP3 and Caspase-1 in the skin were significantly decreased (P<0.05). Conclusion The mechanism of Liangxue Tuizi Formula in the treatment of Henoch-Sch?nlein purpura may be related to the inhibition of ROS-mediated NLRP3 inflammasome activation.
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Progress in the cryopreservation protocols of adipose-derived stem cells

LIU Qin, ZHU Yiliang, CHEN Fang, YU Jing, YANG Lijun, ZHANG Yi

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Adipose derived stem cells(ASCs) become one of the hot seed cells in tissue engineering because of their unique advantages. An ideal method of cryopreservation of ASCs is the goal that researchers have been working on. So far, a lot of researches on cryopreservation protocols of ASCs have been done. In this review, the basical cryobiology and cryopreservation protocols of ASCs were summarized. We also looked forward to the future research interest of cryopreservation protocols of ASCs.
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Exploring the Molecular Mechanisms of Moxibustion Treatment for Osteoporosis Model Rats Using MicroRNA Sequencing Technology

Cui Lu, Li Xiao, Li Xing, Chen Xiaoli, Hu Xiaoshen, Zhou Haiyan, Li Xiang

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Objective: Based on high-throughput sequencing technology for micro-RNA (miRNA), this study explores the molecular mechanisms of moxibustion in improving osteoporosis in rats. Methods: A total of 18 female SD rats were randomly divided into a sham operation group (6 rats) and an operation group (12 rats). The operation group was subjected to ovariectomy to induce osteoporosis (OP), and the 12 rats with successful modeling were randomly divided into a model group and an moxibustion group, with 6 rats in each group. The moxibustion group rats were treated with moxibustion at the “Shenshu” (BL23) and “Guanyuan” (CV4), once a day, for 20 minutes each time, for 12 weeks. Micro-CT scan the rat femur and image it, analyze the trabecular thickness (Tb.Th), trabecular separation (Tb.Sp), and bone volume fraction (BV/TV) of the trabecular bone, and HE staining was used to observe the morphology of tibia tissue. Serum alkaline phosphatase (ALP) and osteocalcin (OCN) levels were measured using ELISA. Three randomly selected rats from each group were used for miRNA high-throughput sequencing, and differentially expressed miRNAs were screened. The functional enrichment analysis and target gene prediction were performed for the differentially expressed miRNAs. Results: The Micro-CT images showed that the bone density of the moxibustion group was superior to that of the model group, and compared to the model group, the moxibustion group showed a significant increase in the thickness of the trabecular bone (Tb.Th), a significant rise in the bone volume/tissue volume (BV/TV) score, and a significant decrease in the trabecular separation (Tb.Sp) (P < 0.05). The ELISA results indicated that compared to the model group, the moxibustion group showed a significant decrease in serum ALP activity and a significant increase in serum OCN content (P < 0.05). The miRNA sequencing results showed that 34 miRNAs were commonly expressed between the model group and the intervention group, and 15 miRNAs were commonly expressed between the model group and the intervention group. The KEGG pathway enrichment analysis showed that the expression of different genes was mainly enriched in signaling pathways such as MAPK, Ras, FoxO, TNF, and cancer-related microRNAs. For the top 5 differentially expressed microRNAs with the highest significance, namely miR-153-5p, miR-201-5p, miR-449c-5p, miR-451-3p, and miR-153-3p, target gene predictions yielded 10 major targets: Ebf2, Rtn4, Fbxl3, Naa15, Vamp2, Daam1, Akap6, Camta1, Ptprz1, and Lamp1. Conclusion: Acupuncture can slow down the progression of OP, improve bone microstructure, and balance bone metabolism. This therapeutic effect may be achieved by regulating the expression of microRNAs and their target genes, and a more detailed mechanism awaits further exploration.
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The effect of Yishen Zhuyu Tongluo Decoction on chondrocyte pyroptosis and ferroptosis in rats with knee osteoarthritis

Wang Jingya, yan kang, Li Ji-an, Wang Meng, Yang Yuyang, Yu Yueyue

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Objective: To investigate the effects of Yishen Zhuyu Tongluo Decoction on chondrocyte pyroptosis and ferroptosis in knee osteoarthritis (KOA) rats. Method: Anterior cruciate ligament dissection (ACLT) was used to create a KOA model in SD rats. The successfully modeled rats were randomly divided into a model group, a celecoxib group, and a traditional Chinese medicine group. Each group received medication intervention on the second day of modeling, for a total of 8 weeks. HE and safranin O staining were used to observe the pathological changes of articular cartilage; ELISA detection of serum IL-1β, IL-18; Micro CT analysis of bone microstructure. RT-PCR detection of MMP13, NLRP3, ASC, Caspase-1, GSDMD, IL-1β, IL-18, ACSL-4, FTH-1, GPX-4, and COX-2. immunohistochemical detection of NLRP3, Caspase-1and COX-2. Result: Compared with the sham surgery group, the expression levels of NLRP3, ASC, Caspase-1, GSDMD, IL-1β and IL-18 in the cartilage tissue of the model group were increased, the expression levels of ACSL-4 and COX-2 of model group rats were significantly increased, while the expression levels of FTH-1 and GPX-4 were significantly decreased. Compared with the model group, the NLRP3, ASC, Caspase-1, GSDMD, IL-1β and IL-18 expression levels of rats in the traditional Chinese medicine group were decreased, the expression levels of ACSL-4 and COX-2 of rats in the traditional Chinese medicine group were decreased, while the expression levels of FTH-1 and GPX-4 were increased. Conclusion: Yishen Zhuyu Tongluo Decoction could treat KOA by inhibiting chondrocyte pyroptosis and ferroptosis in KOA rats, reducing the level of serum inflammatory factors, and improving bone microstructure.
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The Latest Research Progress On The Effects Of Mitochondrial Damage On Cardiomyocytes

FAN Aixue, LIU Meilan

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Cardiovascular disease is still an important cause of death and morbidity worldwide. Mitochondria are considered key organelles in cardiac physiology, accounting for 1/3 of the volume of cardiomyocytes. They are not only the power plant of cardiomyocytes, but also the center of signal transmission, which determines the survival and death of cells, and are potential targets for improving cardiac function. Recent studies have shown that mitochondria are closely related to cell activities such as apoptosis, reactive oxygen species (ROS) production and lipid metabolism, so mitochondrial damage plays an important role in the pathogenesis of cardiovascular diseases (CVD). The purpose of this review is to elucidate the effects of mitochondrial damage (such as mitochondrial autophagy, mitochondrial dynamics) on cardiomyocytes.
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Exploration of Batch Identification Methods for Model Mice

Jin You, Ni Lan, Wei Qi, Zhao Huan, He Jingang

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Objective To establish a simple，fast and economic total DNA extraction method to serve the rapid identification of model mouse genotype in large number of mice. Methods Four methods，i.e.alkali boiling routine method, alkali boiling simplified method, protease K lysis and DNA extraction kit methods were used to extract the total DNA from transgenic mice tails．The purity and concentrationof DNA obtained by the four methods were measured, the advantages and disadvantages of gel electrophoresis were evaluated, and the time-consuming and experimental costs of the four methods were compared．Results The DNA concentration extracted by protease K cleavage method is the highest, followed by alkaline boiling simplified method and conventional method; The DNA purity obtained from the reagent kit treatment is relatively high, followed by the alkaline boiling simplification method. The DNA templates obtained by four methods can be amplified by PCR and Gel electrophoresis to obtain clear DNA target bands, and can also be used for gene identification after being stored at -20 ℃ for one month. In addition, the simplified alkaline boiling method has the lowest cost and the least time consumption. Conclusion The alkaline boiling simplification method is currently the fastest and most economical DNA template extraction method for batch genotyping of model mice.
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5-aza-2 "-deoxycytosine reverses PMT by inhibiting Epo gene promoter hypermethylation in rat primary renal myoblasts______________________________________________________________

yuan ling, wang lei, CHENG Peng, JIANG Qian, CUI Xiao-xue

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Objective To observe the effect of demethylating agent 5-aza-2 "-deoxycytidine (5-Aza-CdR) on pericyte-myofibroblast transition(PMT)of primary rat renal myofibroblast. Methods Rat primary renal myofibroblast were treated with 5-Aza-CdR 250 ng/ml for 72h, and the methylation degree of Epo promoter was detected by pyrosequencing. The protein expression levels of α-SMA, PDGFRβ and DNA methyltransferase (DNMT3a) were detected by immunofluorescence and Western blot, and EPO levels in the supernatant were detected. Results Compared with control group, 5-Aza-CdR treatment significantly decreased the expression of Dnmt3a and the hypermethylation level of Epo promoter, and subsequently decreased the expression of α-SMA and the expression ratio of α-SMA to PDGFRβ in myofibroblast. Meanwhile, 5-Aza-CdR treatment increased the level of EPO in the cell supernatant. Conclusions 5-Aza-CdR can reverse PMT by inhibiting Epo promoter hypermethylation in primary renal myofibroblast.
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Exploration of a behavioral model of motivation deficiency in rats and the role of dopamine receptors in the nucleus accumbensZHANG Jianjun1,3, WU Shuang2, XUE Bing3, ZHANG Lulu1, YU Ping2

zhangjianjun, wushuang, xuebing, ZHANG LULU, yuping

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In recent years, “lie flat” is a buzz word which describes a special psychological state of some people, but its animal behavioral models are lacking, and its psychological meaning and mechanisms remain unclear. Lack of motivation under certain conditions may be one of the key psychological characteristics for “lie flat”. In this study, a novel rat behavioral model of “lie flat” was designed and was used to explore the possible effects of dopamine receptor in the nucleus accumbens on motivation deficiency in “lie flat”.
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Lentinan inhibits TNFα-ferritinophagy and antagonizes hepatic ferroptosis in Sodium arsenite exposed mice

Yuan Yang, Bao Jiacheng, Deng Yekang, Chen Yang, He Qin

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Objective: To explore the intervention effect and mechanism of Lentinan (LNT) on liver ferroptosis in mice exposed to sodium arsenite (SA). Methods: C57BL/6 male mice as experimental subjects, The experiment was divided into control group, SA low-dose group, SA high-dose group, and LNT intervention+SA high-dose group. Biochemical methods and Hematoxylin eosin (HE) staining of liver tissue were applied to evaluate hepatic pathological damage; Enzyme linked immunosorbent assay (Elisa) was used to detect the levels of tumor necrosis factorα (TNFα), microtubule associated protein 1 light chain 3B (MAP1LC3B), Interleukin-6 (IL-6), glutathione peroxidase 4 (GPX4), and iron ions (Fe); Immunoblotting (WB) or immunoprecipitation (IP) methods were used to detect the levels of ferritin heavy chain (FTH1), ratio of LC3B to LC3A, or the co-expressions of FTH1 and LC3, or FTH1 and ubiquitin (Ub); Molecular docking software was applied to analyze the interactions between mitochondrial ferritin (FTMT) and LC3A, LC3B, or Ub. Results: Compared with control group, SA exposure group exhibited hepatic pathological damage and the elevated levels of AST, ALT, TNFα, and IL-6, and the elevated ferritinophagy markers LC3B, FTH1, and Fe, while the levels of ferroptosis biomarkers GPX4 decreased (P<0.05); Compared with SA exposure group, LNT intervention showed a significant reduction in hepatic pathological damage, and showed the downregulations of AST, ALT, TNFα, IL-6, LC3B, FTH1, and Fe, while the level of GPX4 upregulated (P<0.05); WB or IP experiment showed that SA exposure induced the upregulated levels of FTH1 and LC3B/A, and the higher co-expressions of FTH1 and LC3B or Ub protein compared to control group, while LNT intervention showed the downregulated levels of FTH1 and LC3B/A, and the decreased co-expressions of FTH1 and LC3B or Ub protein compared to SA exposure group (P<0.05). Molecular docking simulations showed that FTMT binds stably to LC3A, LC3B or Ub by hydrogen bond. Conclusion: Lentinan antagonizes against sodium arsenite exposure mice hepatic injury and ferroptosis, which may be associated with the inhibition or TNFα-ferritinophagy signaling.
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Coinfection of Coxsackievirus A6 and B1 Experimental Study on Syrian Hamsters Animal Model

houjinghan, duansuqin, xuhongjie, sunwenting, limingxue, liyanyan, jinweihua, chenlixiong, liuquan, zhaoyuan, yangfengmei, hezhanlong

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Objective To establish an animal model of hand, foot and mouth disease (HFMD) in Syrian hamsters coinfected with Coxsackievirus A6 (CVA6） and Coxsackievirus B1 (CVB1）. Methods Twenty-four Syrian hamsters were divided into CVA6 infection group, CVB1 infection group, CVA6 and CVB1 coinfection group and control group. The model was established by nasal instillation of virus solution and PBS. Clinical indicators, physiological indicators, and detoxification status were monitored and recorded for 15 days, and animals were selected on D7 after infection for histopathology and viral antigen and nucleic acid testing. Results Hamsters in the single and coinfection groups showed clinical symptoms similar to human HFMD. The results of WBC, NEUT and LYMPH indicated the blood characteristics of viral infection. Both viral nucleic acids were detected in throat swabs, feces, blood and tissues. Both viruses were isolated in fecal samples. Pathological damage and positive co-localization of CVA6 and CVB1 viral antigen proteins and nucleic acids were found in brain and other tissues. Conclusion The nasal instillation of CVA6 and CVB1 mixture can successfully coinfect Syrian hamsters, replicate herpes similar to human hand, foot and mouth disease, and cause viral myocarditis and encephalitis pathological damage. The results showed that the coinfection group was more serious than the single infection group, with worse clinical symptoms, increased viral replication and obvious tissue pathological damage. This study provides a certain reference for the basic and clinical research of human enterovirus coinfection.
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Study on the establishment of rat model of pelvic inflammatory disease by non-surgical uterine injection

pan xiao yan

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【Abstract】 Objective To establish an efficient and stable model of pelvic inflammatory disease in rats by non-surgical method and evaluate its application in pharmacodynamic test. Methods Female SD rats were randomly divided into control group, model group treated with phenol for 7 days, model group treated with phenol for 10 days, Chinese medicine treatment group with phenol modeling, model group with low concentration of bacterials, model group with high concentration of bacterias and Chinese medicine treatment group with bacterial modeling. SD rats in model group or treatment group were injected with 25% phenol gel, 2×107 or 2×108 Escherichia coli and Staphylostreptococcus aureus mixture by non-surgical method to construct the rat model of pelvic inflammatory disease. The rats in the treatment group were gavaged with Qingpen Huoxue decoction, and the rats in the control group were given the same volume of solvent solution at the same time. The health status, weight change and uterine appearance of rats were observed. The uterine coefficient was calculated. HE staining was used to detect pathological changes of uterus and fallopian tube, endometrial thickness and number of glands. Serum levels of IL-1β, IL-6 and TNF-α were detected by ELISA. Macrophage marker CD68 protein expression was detected by immunofluorescence staining. The expression of TLR4/NF-KB pathway-related proteins in the uterus of rats was detected by western blotting. Results The mortality rate in the model group was only 5%. Compared with the control group, the body weight of rats decreased, uterine coefficient increased, pathological changes of uterus and fallopian tube appeared in different degrees, endometrium thinned, the number of glands decreased, serum levels of IL-1β, IL-6, TNF-α and the number of macrophages in uterine tissue increased significantly, and TLR4/NF-kB signaling pathway was activated. The 7-day phenol model and low-concentration bacterial solution model were judged to be mild pelvic inflammatory disease model, and the 10-day phenol model and high-concentration bacterial solution model were judged to be severe pelvic inflammatory disease model. After the treatment of Chinese patent medicine--Jingangteng, the pathological symptoms of uterus and fallopian tube were obviously relieved, which was in line with the efficacy evaluation of clinical pelvic inflammatory disease. Conclusion The rat model of pelvic inflammatory disease established by using phenol and mixed bacterial solution in non-surgical method can better simulate the different pathological states of pelvic inflammatory disease caused by different causes, which is suitable for drug efficacy evaluation and elucidating the pathological mechanism of pelvic inflammatory disease.
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Regulatory role of KHSRP in lung adenocarcinoma: Key role of JAK1/STAT3 pathway

Ma Chaonan, Wang Mengyao, Liu Yangyang, lili, Wei Haitao

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Objective To investigate the effect of KHSRP on the malignant biological behavior of lung adenocarcinoma by targeting JAK1/STAT3 signaling axis. Methods The clinical data of 64 cases of LUAD tissues and adjacent tissues diagnosed in Huaihe Hospital from January 2017 to December 2018 were collected. The expression level of KHSRP in LUAD tissues and adjacent tissues was observed by immunohistochemical staining. qRT-PCR was used to detect the expression of KHSRP in lung adenocarcinoma cell lines (SPC-A1, H1975, CL1-5, PC-9, Calu-3, H446) and normal human bronchial epithelial cell line (NHBE). Lentivirus transfection changed the expression of KHSRP in lung adenocarcinoma cell lines SPC-A1, H1975, PC-9 and Calu-3. Cell counting kit-8 (CCK-8) and Transwell assay were used to determine the effect of KHSRP on the proliferation, migration and invasion of lung adenocarcinoma cells. Detection to knock down and xenograft tumor model expression KHSRP in living animals. WB experiment KHSRP targeted JAK/STAT signaling pathway. Rescue experiment was conducted to verify whether KHSRP promotes malignant progression of LUAD cells by regulating JAK1/STAT3 signaling pathway. Results Compared with adjacent normal tissues, KHSRP expression in LUAD organizations significantly higher (P<0.05). Overexpression of KHSRP significantly promoted the proliferation, migration and invasion of LUAD cells in vitro (P<0.05). The results of in vivo animal experiments showed that KHSRP can promote LUAD cell xenograft tumor growth and lung nodule metastasis in nude mice (P<0.01). After KHSRP knockdown, the levels of JAK1, p-JAK1 and STAT3 in JAK/STAT signaling pathway were significantly decreased, while the situation was opposite after KHSRP overexpression (P<0.05). Rescue experiment showed that KHSRP can reverse the inhibitory effect of knockdown (P<0.05). Conclusion KHSRP targets JAK1/STAT3 signaling pathway and acts as an oncogene in lung adenocarcinoma.
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Comparative experimental study of sodium benzoate and corticosterone in a mouse model of asthenozoospermia with high SDF

Lu zong lin, Zhao hai yang, Wang hui, Wang xin, Sun zi xue

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【】? Objective? The preparation of an animal model of asthenozoospermia with hypersperm DNA fragmentation was explored by inducing the construction of a mouse model of asthenozoospermia (AZS) with hypersperm DNA fragmentation (SDF) by the hormone corticosterone (CORT) and the compound sodium benzoate (NaB).? Methods? Fifty 3-week-old male ICR mice were randomly divided into 30 CORT-treated groups and 20 NaB-treated groups. The CORT treatment group was divided into 6 groups, with 5 animals in each group, of which 3 groups were high (500 μg/ml), medium (200 μg/ml) and low (10 μg/ml) dose groups of CORT drinking water modeling, 1 group was drinking water control group, 1 group was CORT injection molding group (40 mg/kg), and 1 group was injection control group (normal saline), and the model was continuously modeled for 50 days. The NaB treatment group was divided into 4 groups, with 5 animals in each group, of which 3 groups were high (500 mg/kg), medium (300 mg/kg) and low (100 mg/kg) NaB gavage groups, and 1 group was control group (normal saline), and the model was continuously modeled for 50 days. The physiological state of the mice in each group was observed and the weight changes were continuously recorded, and the sperm motility capacity and DNA fragmentation index (DFI) of the sperm were observed from the tail of the epididymis of the mice after the end of the modeling. Results? The rate of weight change in the CORT injection group showed a downward trend, There was no significant difference (P>0.05) in the high-dose NaB gavage group, and the change rate of body weight in the high-dose NaB gavage group decreased significantly compared with the control group (P<0.05), the percentage of forward motility sperm in the CORT injection group decreased compared with the control group (P>0.05), the percentage of forward motility sperm in the high-dose NaB gavage group decreased significantly compared with the control group (P<0.05), the DFI in the CORT injection group increased with no significant difference compared with the control group (P>0.05), and the DFI in the high-dose NaB gavage group increased significantly compared with the control group (P>0.05).? Conclusion? Intragastric gavage at NaB 500mg/(kg·d) for 50 days is an ideal method to construct an animal model of AZS with high SDF.
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Research on the Potential Mechanism of Pepper Extract Regulating Ferroptosis and Alleviating Depression

GUAN Dongyan, ZHANG Mijia, HOU Zhiying, WANG Jiayin, YU Jiawei, FAN Bei, XIE Hui, DUAN Zhouwei, BAI Yajuan, WU Honghong, WANG Fengzhong, WANG Qiog

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Abstract: Objective Using network pharmacology and molecular docking techniques to predict the potential mechanism by which active components in Piper (Piper nigrum L., PN) regulate ferroptosis to alleviate depression. Methods Firstly, the chemical composition of Piper was obtained from the Traditional Chinese Medicine System Pharmacology Database (TCMSP), and disease-related genes were obtained using the Online Mendelian Inheritance Database for Humans (OMIM), Genecards, and FerrDB databases. The active ingredient-target-disease network was mapped using Cytoscape software, the protein interaction network (PPI) was mapped using the STRING database, and gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were carried out using the open-source bioinformatics software Bioconductor. Next, molecular docking was conducted to validate the binding capacity between the core targets and their corresponding active components. Finally, we established a chronic restraint stress (CRS) mouse model, treated with different concentrations of PN (75, 150, and 300 mg/kg) for four weeks, followed by behavioral assessments and qPCR to verify the expression of core genes. Results We identified nine active components from PN, corresponding to 27 targets. There are 8,377 targets related to depression and 547 targets related to ferroptosis, resulting in an intersection of 25 target genes. KEGG enrichment analysis revealed that these core targets are primarily enriched in signaling pathways such as cholinergic synapses, serotonergic synapses, and neuroactive ligand-receptor interactions. Molecular docking results indicate that the main active components of PN exhibit strong binding affinity with the targets CHRM2, SLC6A4, PTGS2, and SLC6A2. Behavioral assessments demonstrated that PN significantly increased the saccharin preference index in treated mice, reduced immobility time in the tail suspension and forced swimming tests, and enhanced exploratory behavior in the open field test. Neurotransmitter analysis revealed that PN significantly elevated serotonin and acetylcholine levels in the hippocampus of mice. qPCR results showed that PN can downregulate the mRNA expression of SLC6A4 and PTGS2. Conclusion PN may regulate ferroptosis and improve depressive-like behavior in mice by modulating serotonin and acetylcholine levels, participating in immune regulation, and exerting neuroprotective effects.
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Research advances on Iron overload and related Animal models

TANG Huian, AO Guangyu, CHEN Min, ZHANG Yujiao, CHEN Zejun

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Iron is an essential trace element for the human body, critical for vital cellular processes such as DNA synthesis, respiration, and oxygen transport. The body meticulously maintains iron homeostasis through a coordinated balance of absorption, utilization, storage, and distribution. Both iron deficiency and excess can lead to pathologies; the latter can trigger lipid peroxidation and DNA mutations through the Fenton reaction, potentially causing iron-induced cell death in severe cases. Iron overload is recognized to inflict significant damage on multiple organs, including the brain, liver, spleen, heart, ovaries, and kidneys. Despite this, the mechanisms that regulate iron homeostasis in response to overload are not fully understood.To elucidate these mechanisms, various animal models have been developed, each reflecting different aspects of iron overload (IOL) relevant to human diseases. Accurately simulating the pathological and physiological states associated with human IOL-related diseases necessitates the selection of the most appropriate animal models. This review synthesizes recent literature on animal models pertinent to iron overload, aiming to offer insights for the development and analysis of models for diseases related to iron overload.
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Research progress on the role of common vitamins and elements in the treatment of Alzheimer's disease

Wujianfei

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Alzheimer"s disease (AD) is a neurodegenerative disease caused by a variety of risk factors, which is the main cause of dementia in the old people. At present, the pathogenesis of AD has not been studied clearly, and the treatment of AD is very limited. Clinical drugs can only alleviate the symptoms of AD to a certain extent, but can not delay the course of AD. At present, the pathogenesis of AD has not been studied clearly, and the treatment of AD is very limited. Clinical drugs can only alleviate the symptoms of AD to a certain extent, but can not delay the course of AD. A large number of studies have shown that a variety of micronutrients play a positive role in the treatment of AD. Vitamins, trace metal elements, unsaturated fatty acids and polyphenols have many functions such as anti-inflammation, anti-oxidation and protection of mitochondria. Micronutrients can effectively reduce Aβ protein plaque deposition and Tau protein hyperphosphorylation to improve brain energy metabolism, thereby achieving the prevention and treatment of AD. The purpose of this article is to explore the mechanism of micronutrients in the treatment of AD, and to review its application and effect in the treatment of AD, and to provide theoretical basis and new strategies for micronutrient intervention in the treatment of AD.
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Proton Pump Inhibitor Pantoprazole Promotes Colonization of Helicobacter pylori SS1 in Mouse Stomachs

Shuo Yan, Xue Li, Chao Wang, Jiali Xu, Yu Cheng, Liping Zhang, Lei Su, Jianan Gong

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Objective To explore methods for improving the colonization efficiency of Helicobacter pylori (Hp) in the mouse stomach and to determine whether the proton pump inhibitor (PPI) pantoprazole can act as a colonization adjuvant to enhance Hp colonization. This study aims to provide an effective tool for establishing an Hp infection mouse model. Methods The Hp Sydney strain (SS1) was introduced, and solid plate and liquid culture systems were established and identified. The effects of different doses of pantoprazole on gastric acid secretion in mice were compared. The impact of Hp inoculation alone or combined with pantoprazole pretreatment on Hp colonization efficiency was analyzed using rapid urease tests, bacterial plate cultures, and TaqMan qPCR. Results Proton pump inhibitor pretreatment inhibited gastric acid secretion and, to some extent, promoted Hp colonization in the mouse stomach. Conclusion Proton pump inhibitors can serve as colonization adjuvants to enhance the efficiency of constructing Hp infection mouse models.
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Effects of circadian rhythm on mood and cognitive behavior in male and female mice under chronic restraint stress

qiangmeng, jiangning, huanghong, zhangyiwen, chenfang, lizhaohui, liuxinmin, lvguanghua

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Objective To investigate the effects of chronic restraint stress for 28 days during the day and night on the mood and cognitive-like behavior of male and female ICR mice, so as to provide a basis for the selection of sex and restraint period in experimental animals in the chronic restraint stress model. Methods ?A total of 72 male and half ICR mice were divided into 6 groups: male blank control group, male daytime restraint group, male nighttime restraint group, female blank control group, female daytime restraint group, and female nighttime restraint group. Except for the blank control group, the other groups were bound for 10 h every day and continuously restrained for 28 days to establish a chronic restraint stress model. The emotional and cognitive behaviors induced by restraint in male and female ICR mice at different times were observed by empty field experiment, Y maze experiment, novel inhibition feeding experiment, elevated cross maze experiment, tail suspension experiment, forced swimming experiment, and dark avoidance experiment. Results In the tail suspension experiment, the immobility time of the male mouse in the daytime restraint group was significantly increased compared with that in the blank group (P<0.05). In the forced swimming experiment, the immobility time of the daytime and nocturnal restraint groups of male mice was significantly increased compared with that of the blank group (P<0.05). In the novelty inhibition feeding experiment, there was no significant difference between the daytime binding group and the blank group, and the feeding latency of the nighttime binding group was significantly longer than that of the blank group (P<0.05) and significantly longer than that of the daytime binding group (P<0.05), and the feeding latency of female mice was significantly longer than that of males during nocturnal binding (P<0.05). In the empty field experiment, the central zone time and central zone time compared with the male blank group were significantly decreased compared with the blank group (P<0.05), the central zone time and central zone time compared with the blank zone were significantly decreased compared with the blank group in the female mice (P<0.05), and the central zone time and central zone compared with the margin zone of the female mouse blank group were significantly increased compared with the male blank group (P<0.05). There was no significant difference between the groups in the elevated cross maze experiment and the Y maze experiment. In the dark avoidance experiment, there was no significant difference between the dark latency of the daytime restraint group and that of the blank group, and the darkness latency of the nighttime restraint group was significantly shortened compared with that of the blank group (P<0.05). Conclusions Male mice exhibit depression after 28 days of chronic restraint stress during the daytime. After 28 days of chronic restraint stress, female mice were prone to anxiety. Learning and memory impairment occurred in male mice after 28 days of chronic restraint stress during the night period.
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Exploring the Mechanism of Modified Jisheng Shenqi Decoction in Improving Hypoxia Microenvironment and Preventing Cirrhosis Based on HIF-1 α/Notch Signaling Pathway

moyiling, zhouxiaoling, liulin, sundongqi, wuteng, luoyi, ruanbowen, wangyueming, jiayao

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Objective: To explore the mechanism of Jiawei Jisheng Shenqi Decoction in improving the hypoxic microenvironment and antagonizing liver cirrhosis. Method: In vivo experiments were conducted on a rat model of liver cirrhosis induced by carbon tetrachloride. Normal group, model group, colchicine group, and low, medium, and high dose groups of Jiawei Jisheng Shenqi Decoction were set up. HE staining and Masson staining were used to observe the pathological changes in liver tissue of rats in each group;Test kit was used to to detect changes in serum liver function in each group of rats; Elisa was used to detect the levels of hyaluronic acid (HA), laminin (LN), procollagen III (PCIII)and collagen type IV(COL4) in each group of rats; Western blot was used to detect the expression of hypoxia inducible factor-1α(HIF-1α), Notch1, Jagged1, and α-smooth muscle actin(α-SMA) proteins in rats. In vitro experiments were conducted on HSC-T6 cells, and the CCK-8 method was used to screen for the most suitable (100 μM, 200 μM, 400 μM, 600 μM, 800 μM) concentrations of CoCl2 cultured cells and the optimal intervention concentrations of drug containing serum (5%, 10%, 15%, 20%); Scratch test was used to detect the migration ability of cells in each group; Flow cytometry was used to detect changes in apoptosis rate of cells in each group; Western blot was used to detect the expression of HIF-1α, Notch1, Jagged1, a-SMA, Matrix Metallopeptidase 9(MMP9), and Tissue Inhibitor of Metalloproteinases 1(TIMP-1) proteins in each group of cells. Results：In vivo experiment: Compared with the control group, the model group rats showed significantly increased liver swelling, inflammatory cell infiltration, and collagen deposition, as well as the appearance of pseudolobules. The levels of serum ALT, AST, HA, LN, PCIII, COL4 were significantly increased, while ALB was significantly decreased. The expression of HIF-1α, Notch1, Jagged1, and α-SMA proteins in liver tissue was significantly increased (P<0.01). Compared with the model group, the liver swelling, inflammatory cell infiltration, and collagen deposition in each treatment group rats were significantly reduced, and the degree of fibrosis was reduced. The levels of serum ALT, AST, HA, LN, PCIII, COL4 were significantly decreased, while ALB was significantly increased. The expression of HIF-1α, Notch1, Jagged1, and α-SMA proteins in liver tissue was also significantly increased. Decreased to varying degrees (P<0.05). In vitro experiments: Hypoxia can promote HSC-T6 migration, reduce HSC-T6 apoptosis, and increase the expression of HIF-1α, Notch1, Jagged1, a-SMA, and TIMP-1 proteins, while reducing the expression of MMP9 protein (P<0.01). The serum containing Jiawei Jisheng Shenqi Decoction can inhibit HSC-T6 migration, promote HSC-T6 apoptosis, and lower the expression of HIF-1α, Notch1, Jagged1, a-SMA, and TIMP-1 proteins, while enhance the expression of MMP9 protein (P<0.01). However, its inhibitory effect on HSC-T6 cell activation can be reversed by the HIF-1 α agonist DMOG. Conclusion: Jiawei Jisheng Shenqi Decoction can improve the hypoxic microenvironment through the HIF-1α/Notch pathway, thereby exerting an anti liver cirrhosis effect.
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Application and research progress of electroencephalographic resting microstates in generalized anxiety disorder

LI Chenrui, WU Yiming, CHEN Xinwang, HE Yayong, NAN Shanzhu

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In recent years, the incidence of generalized anxiety disorder (GAD) is at an increasing stage year by year in a complex social environment. Currently, the diagnosis of GAD often relies on DSM-5 and ICD-10 criteria, which have certain subjectivity and limitations. Understanding the intrinsic activity of brain network function and structural connectivity has proven to be an important goal of contemporary neuroscience research. EEG microstates are capable of observing broad frequency components and capturing dynamic changes in brain activity as a way to provide a new way of thinking about the accuracy of GAD diagnosis. This paper delves into the EEG microstate features and explores the abnormalities in the functional brain network of GAD patients, aiming to further provide a clear diagnosis, optimize the therapeutic efficacy and improve the quality of medical care for GAD patients.
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Research Progress on the Role and Mechanisms of Epigenetics in Delirium Diseases

xuxinyi

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Delirium has a high incidence and is prone to lead to poor prognosis of patients. The pathogenesis is still not completely clear, and antipsychotic drugs are mainly used to intervene in clinical practice, and there is no drug that can definitively improve the long-term health-related quality of life of patients with delirium. In this study, we review the research on the association between epigenetic modifications such as non-coding RNA, DNA methylation, histone acetylation and the development of delirium, with the aim of providing clinical decisions on the early identification and diagnosis of delirium, its treatment and prognosis, and the development of relevant targeted drugs.
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Research Progress on The Biomarkers of Drug Addiction

HUANG Wenxin, ZHANG Qianyao, LI Xiaodong, TIAN Yunqing, HUANG Jian, ZHANG Rui-lin

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Drug addiction is a chronic disease that not only causes serious physical and psychological harm to the individual, but more importantly, it also causes serious damage to society. Biomarkers are indicators that differ significantly between healthy people and patients, and are important for both diagnosis and treatment of diseases. Due to the increasing number of drug-addicted patients in recent years and the increasing variety and number of new drugs, the study of biomarkers of drug addiction has been increasing, and biomarkers are present in different biological samples. This paper reviews the biomarkers in hair, blood, urine and faeces, which can help to explore the biosignature markers of drug addiction and facilitate the clinical diagnosis and treatment of drug addiction.
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Effects of five-element music on depressive behaviors and intestinal flora of stress-phobic offspring during pregnancy

lixiaolin, yangliping, houjunlin, wangyaohui, yuchenyang, lilingling

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Objective Exploring the effects of five-element music on depressive behavior and gut flora of stress-phobic offspring during pregnancy. Methods Thirty-six 0.5-day pregnant Wistar female rats were randomly divided into the blank group, the stress-phobic group and the five-element music group, and the litters were continued in the maternal group. Pregnant rats in the 1-19 day gestation stress-phobic group and the five-element music group were modeled by the side-by-side electroshock method, while the five-element music group was given the five-element music feathering intervention. The effect of modeling was evaluated by using the absent field experiment, enzyme-linked immunosorbent assay (ELISA) to detect the fearful behavior and serum glucocorticoid (GC) content of the pregnant rats on the 20th day of gestation; the depressed mood of the rats was evaluated by using the absent field experiment, the tail-hanging experiment and the sugar-water preference experiment at the age of 3 weeks; and the changing pattern of the intestinal flora of the rats was analyzed by using 16S rRNA sequencing. Results Compared with the blank group, pregnant rats in the stress-phobic group stayed longer in the peripheral area of the absent field, had fewer entries into the central area (p < 0.05), and had higher serum GC levels (p < 0.001), whereas the five-element music group reversed the behavioral changes in the stress-phobic group (p < 0.05) and the serum GC levels (p < 0.001). Compared with the blank group, the stress-phobic group showed a decrease in the number of absentee grids worn (p < 0.01), a decrease in the glycemic index, and a prolongation of the time of tail suspension (p < 0.05), while the five-element music group showed an increase in the number of absentee grids worn, the glycemic index, and a shortening of the time of tail suspension (p < 0.05), and the total distance traveled by the rats in each group did not show any significant difference. The intestinal flora species diversity of the rats in the stress-phobic group decreased (p < 0.01) and the structure of the flora was significantly changed compared with that of the blank group, in which the abundance of Proteobacteria, Enterobacteriaceae, Enterococcus and Escherichia were up-regulated, and the abundance of Spirochaetes and Spirochaetaceae, Lachnospiraceae, Ruminococcaceae,Treponema, Prevotella,Coprococcus, Allobaculum, Ruminococcaceae_Ruminococcus, Dorea was down-regulated, and five-element music group of littermates showed an increase in species diversity of the intestinal flora compared to the stress-phobic group (p < 0.01) and reversed the changes in the abundance of the above flora. Conclusion A five-element music intervention during pregnancy is effective in ameliorating fearful stress-induced depression behavior and gut flora disruption in offspring during pregnancy.
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Neuroprotective effect of Dendrobium nobile Lindl extract on Caenorhabditis elegans model of Parkinson"s disease

FAN Xinyue, HE Wenlu, DONG Li, HOU Zhiyin, ZHENG Hanwen, Alberto Carlos Pires Dias, WANG Qiong

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Objective To investigate the effect of Dendrobium nobile Lindl (DNL) on Caenorhabditis elegans (C. elegans) model of Parkinson"s disease, 6-OHDA was used to induce C. elegans model of Parkinson"s disease(PD), and Dendrobium nobile was used to interfere with C. elegans. Methods C. elegans NL5901 and 6-OHDA-induced N2, BZ555, PD4521 and BC7272 were treated with DNL of 7.5, 15 and 30mg/L. The survival rate, basal slowing response rate, α-synuclein aggregation(α-syn), dopaminergic neurons(DNs), mitochondrial distribution density of body wall muscle cells and protein levels in the membrane were observed. In addition, the activity of SOD and GSH in 6-OHDA-induced N2 was detected to explore the effect of DNL on the anti-oxidative stress ability of Parkinson disease C. elegans models. Results Compared with the PD model group, the DNs fluorescence intensity of the nematodes treated with DNL and L-DOPA was significantly increased (P<0.001), α-syn aggregation was significantly decreased (P<0.05 or P<0.001), the basal slowing rate was increased (P<0.05 or P<0.001), mitochondrial density was increased (P<0.001), mitochondrial intima protein content was increased (P<0.05 or P<0.001), SOD(P<0.05) and GSH content are also increased. The lifespans of N2 wild type C. elegans and PD C. elegans models were prolonged after DNL treatment (P<0.05 or P<0.001). Conclusions A certain concentration of DNL can effectively improve the paralysis of C. elegans model of Parkinson"s disease, improve the degeneration of dopaminergic neurons, reduce the accumulation of α-syn and suppressed the loss of DNs. Overall, DNL treatment increase the ability of anti-oxidative stress, and slow down the aging process of C. elegans. These results provide reference for the screening of effective drugs for Parkinson"s disease.
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Exploring the mechanism of action of Gegen QinLian Decoction in improving Non-alcoholic Fatty Liver Disease by inhibiting iron death based on the Nrf2/SCLC7A11/GPX4 pathway

LUO Qian, LUO Tao, SONG Zhenzhen, LIANG Fang, LI Junsen, PENG Shuhong, CAO Lan, ZHAO Haiping, ZHANG Changhua

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Objective To investigate the mechanism of the action of nuclear factor erythroid 2-related factor 2Nrf2/solute carrier family 7 member 11 (SLC7A11)/glutathione peroxidase 4 (GPX4) signaling pathway in NAFLD by in vivo and in vitro experiments. The mechanism of Gegen QinLian Decoction in the treatment of non-alcoholic fatty liver disease (NAFLD) was investigated in vivo and in vitro. Methods Animal experiments: Rats were fed with high-fat chow for 24 weeks to complete the induction modeling of NAFLD, and were randomly divided into normal, model, Gegen QinLian Decoction high-dose, medium-dose, low-dose, and metformin (Met) groups. From the 25th week onwards, the corresponding drugs were gavaged for two weeks according to the grouping until sampling. Biochemical kits were used to measure the levels of oxidative stress: malondialdehyde (MDA) and glutathione (GSH) in the liver tissues of rats in each group. A ferrous ion kit was used to detect ferrous iron (Fe2+) in rat liver tissues. qRT-PCR was used to detect Nrf2, heme oxygenase-1 (HO-1), SLC7A11, glutathione synthetase (GSS), GPX4 and acyl coenzyme A synthetase 4 in rat liver tissues. Glutathione Synthetase (GSS), GPX4 and Acyl Coenzyme A synthase (ACSL4) mRNA expression levels. Cellular experiments: 1 mmol/L free fatty acid (FFA) was used to induce lipid accumulation in hepatocellular carcinoma HepG2 cells mimicking the NAFLD in vitro model, and different concentrations of Gegen QinLian Decoction and metformin-containing serum were added for treatment. Oil red O staining was used to detect the lipid accumulation of cells in each group. Kits were used to determine the MDA and GSH content of HepG2 cells in different groups. Cell-specific ferrous kit was used to detect the ferrous content of cells in each group. qRT-PCR was used to detect the expression levels of Nrf2, HO-1, SLC7A11 , GSS, GPX4 and ACSL4 mRNA in cells of each group. Results Animal experiments: MDA and Fe2+ contents in liver tissues of rats in the model group were significantly higher than those in the blank group, and GSH contents were significantly lower (P<0.01); the Gegen QinLian Decoction high and medium dose groups and the metformin group could substantially reduce MDA and Fe2+ contents and elevate GSH contents, compared with the model group (P<0.01, 0.05). Compared with the model group, the Gegen QinLian Decoction high- and medium-dose groups and the metformin group increased the expression levels of Nrf2, HO-1, GSS, and GPX4 mRNA, and decreased the level of ACSL4 mRNA (P<0.01, 0.05). Cellular assay:Red lipid droplets were significantly increased in the HepG2 cell model group compared with the blank group, and the use of Gegen QinLian Decoction and metformin led to a significant decrease in lipid droplets. The kit assay revealed that MDA and Fe2+ content increased significantly in the HepG2 cell model group, and GSH content decreased significantly compared with the normal group (P<0.01),while all dose groups of Gegen QinLian Decoction and metformin group significantly decreased MDA and Fe2+ content compared with the model group (P<0.01), and the high and middle dose groups of Gegen QinLian Decoction, the low dose group, and the metformin group increased GSH content (P<0.01, 0.05). qRT-PCR experiments showed that the mRNAs of Nrf2, GSS, GPX4, and SLC7A11 in the high dose group of Gegen QinLian Decoction, Nrf2, HO-1, and SLC7A11 in the middle dose group, HO-1, SLC7A11, and GSS in the low dose group, as well as GSS, Nrf2, HO-1 in the metformin group, mRNA expression levels of GPX4 and SLC7A11 were significantly increased compared with the model group (P<0.01, P<0.05). The mRNA expression of ACSL4 was significantly decreased in the middle and low dose groups of Gegen QinLian Decoction and the metformin group (P<0.01, 0.05). Conclusion Gegen QinLian Decoction can improve NAFLD by inhibiting iron death, and its mechanism of action may be related to the regulation of Nrf2/SLC7A11/GPX4 signaling pathway.
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Mechanism of Vagus Nerve Stimulation in the Neuro-regulation of Attention

zhijincao, jiaxueyan, changqing, xuhe, jiweiwei, wangyan

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Attention refers to the body’s capacity to maintain an alert awareness of the internal and external stimuli. Attention deficit can significantly impairs the learning capacity and working proficiency with a heavy burden to the family and society. Vagus nerve stimulation (VNS), as an emerging neuroregulatory technique that can achieve reciprocal interaction between the central and peripheral nervous system, has been found to have great potential in the treatment of neurological and psychiatric diseases. However, it has not been used in the clinic for treating the attention-deficient developmental disorders in children and neurodegenerative diseases in aged population. In this paper, the anatomical and physiological basis of VNS, the application status of VNS, and potential use of VNS in treating attention deficit diseases are briefly reviewed. The potential mechanism of VNS participating in attention nervous regulation is proposed in order to lay a theoretical foundation for the application of VNS in the field of attention nervous regulation.
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Breeding and biological risk control of laboratory monkeys for Animal Biosafety Level 2 Laboratories

Lu Shuangshuang, Li Xiaoyan, Lu Ziwei, Bi Xiang, Lu Xuancheng

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Animal biosafety laboratories generally use negative-pressure cages to raise animals to guarantee biosafety. The monkeys are much larger when compared with the rodents. The monkeys are mostly housed in negative-pressure rearing cages within animal biosafety laboratories in a semi-open form. With practical work experience in an animal Biosafety Level 2 (ABSL-2) laboratory, the author discussed how to control biological risk at various stages of monkey breeding and infectious experiments within the ABSL-2 laboratory. This exploration provides valuable insights and references for controlling biological risks with monkey infectious experiments in ABSL-2 and ABSL-3 laboratories in the future.
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Analysis of Vascular Restenosis Animal Model Based on Data Mining

xiebeili, liumingwang, wenwei, yanyuxin, gaomengjie, jianglulian, jinzhidie, zhaofuhai

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Objective: To analyze the modeling methods and evaluation methods of vascular restenosis animal model in recent 10 years, and provide reference for improving vascular restenosis animal model. Methods: Literature related to vascular restenosis was retrieved from Chinese and English mainstream databases from 2013 to 2023. Data of experimental animal strain, modeling method, modeling cycle and detection method were extracted from the included literature, and a database was established by Excel for summary analysis. Results: Among the 122 articles, the experimental animal strains were mainly rats, rabbits and pigs, and the sex was mainly male. The most commonly used modeling method was balloon injury, and the modeling cycle was mainly within 4W-8W. The detection indexes were mainly histopathology, accounting for 37.18%, including routine hematoxylin-eosin staining, Masson staining and EVG staining. Conclusion: At present, the translatability of porcine vascular restenosis model is more in line with expectations, but the cost is high and it is difficult to popularize. Rats and rabbits are still the mainstream. Balloon injury is the main mode of modeling. Different vascular restenosis animal models and modeling methods have advantages and disadvantages, and should be selected according to the experimental purpose.Animal models of vascular restenosis still have some limitations, and it is inevitable to seek more ideal animal models in the future.
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Overview of the Mechanisms by Which Traditional Chinese Medicine Modulates the NF-κB Signaling Pathway to Alleviate Diabetic Kidney Disease

LI Xin, PAN Zhi

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Diabetic kidney disease (DKD) is a common complication of diabetes mellitus (DM) and a leading cause of end-stage renal disease (ESRD). Increasing evidence indicates that the nuclear factor-kappa B (NF-κB) signaling pathway plays a pivotal role in the onset and progression of DKD. Numerous experimental studies have demonstrated that traditional Chinese medicine (TCM) can attenuate inflammatory responses by modulating the NF-κB signaling pathway, thereby delaying the progression of DKD. This review summarizes the relationship between the NF-κB signaling pathway and DKD, and discusses the advances in research on how TCM interventions targeting the NF-κB signaling pathway can alleviate DKD. The aim is to provide new references for targeted therapy of DKD.
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To compare the changes of depressive behavior in mice induced by different doses of corticosterone injection

ARuHan

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【Abstract】Objective To observe the changes of depressive behavior and neuronal damage induced by different doses of corticosterone (CORT) in mice, and to explore the best dose of corticosterone-induced depression model in mice. Methods Forty male C57BL/6J mice were randomly divided into four groups: normal control group and corticosterone group (low, medium and high, 20, 40 and 60 mg/kg), and the corresponding drug intervention lasted for 4 weeks. The behavioral changes of mice after subcutaneous injection of corticosterone for 3 and 4 weeks were detected by sugar water preference test, forced swimming test, tail suspension test and open field test. Hematoxylin-eosin staining (HE) and Nissl staining were used to observe the morphological changes of neurons in hippocampal CA1 area and forebrain cortex area of mice. Enzyme-linked immunosorbent assay (ELISA) was used to detect the content of 5- hydroxytryptamine (5-HT) in serum. To compare the behavioral changes of depression in mice induced by different doses of corticosterone. Results Compared with the control group, the weight of mice in corticosterone dosage groups (20 mg/kg, 40 mg/kg and 60 mg/kg) decreased (P < 0.05) and the preference of sucrose solution decreased (P < 0.01). The immobility time of forced swimming mice in corticosterone 20 mg/kg and 40 mg/kg groups was prolonged (P < 0.01). The immobility time of mice in the 40 mg/kg corticosterone group was prolonged (P < 0.05). The total distance, the average speed and the times of entering the central area of the open-field experimental mice in the corticosterone 40 mg/kg and 60 mg/kg groups decreased (P < 0.05), and the stay time in the peripheral area of the mice was prolonged (P < 0.05). In addition, corticosterone injection resulted in incomplete neuronal cell morphology, cell deformation and nuclear condensation in hippocampal CA1 area and forebrain cortex area of mice in different degrees. The level of 5-HT in serum of 40 mg/kg and 60 mg/kg corticosterone decreased (P < 0.05). Conclusion Corticosterone at 20 mg/kg, 40 mg/kg and 60 mg/kg can induce depression-like behavioral changes and neuronal damage in mice to varying degrees, and the effect of corticosterone at 40 mg/kg is more obvious. Under the experimental conditions, it is preliminarily considered that 40 mg/kg is the best dose to replicate the depression model induced by corticosterone in mice.
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Research progress of LncRNA in cerebral ischemia/reperfusion injury

huazhipeng, lv xue, li hao, yang zhan jun, jia jian xin, yang zhi fu

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Cerebral ischemia/reperfusion injury (CIRI) is a significant pathophysiological process affecting the prognosis of patients with ischemic stroke. Its mechanism is complicated and has not been completely clarified. Long non-coding RNA (LncRNA) is a class of non-coding RNA (ncRNA). Early studies focused on its relationship with tumor-related diseases. Recent studies have found that, It is also closely related to the pathological process of ischemia/reperfusion injury. Therefore, in this paper, the relevant mechanisms of LncRNA in cerebral ischemia-reperfusion injury were reviewed.
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Preparation of human SET8 monoclonal antibody and its effect on hepatocellular carcinoma cell proliferation, apoptosis and cell cycle

Wang Yingnan, Wu Jianhua, Wu Chensi, Zhang Fengbin, Zhang Ruixing, Guo Zhanjun

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Objective To prepare human SET8 monoclonal antibody and explore its effects on the proliferation, apoptosis and cell cycle of hepatoma cells, and evaluate its anti-tumor effect in mouse models of hepatocellular carcinoma. Methods By immunizing mice with human SET8 polypeptide fragment, B cells and myeloma cells were screened and fused to establish hybridoma cell line that secreted SET8 monoclonal antibody stably. The production was expanded by intraperitoneal injection of mice and collection and purification of ascites. The CCK-8, flow cytometry and Western blot were used to analyze the effects of SET8 monoclonal antibody on the proliferation, apoptosis, cell cycle and apoptosis-related protein expression of hepatocellular carcinoma cells. Finally, a mouse model of human hepatocellular carcinoma cell transplantation was constructed to evaluate the inhibitory effect of SET8 monoclonal antibody on tumor growth in vivo. Results Human SET8 monoclonal antibody significantly inhibited the viability of Huh-7 and Mahlavu hepatoma cells at the concentration of 50ug/ml and 100ug/ml, and the higher the concentration, the stronger the inhibitory effect. Flow cytometry analysis showed that compared with the control group, SET8 monoclonal antibody, paclitaxel and their combination treatment significantly increased the apoptosis rate of Mahlavu cells, and the combination group had the best effect. Meanwhile, SET8 monoclonal antibody induced Mahlavu cell cycle arrest in S and G2 phases and reduced G1 phase cells. Western blot analysis showed that the monoclonal antibody increased the expression of apoptosis-related proteins Bax and caspase-3. Further animal experiments showed that SET8 monoclonal antibody alone or in combination with paclitaxel effectively inhibited the proliferation of hepatocellular carcinoma cells in nude mice, and the combination therapy had the most significant effect. Conclusion The prepared human SET8 monoclonal antibody effectively inhibited the proliferation of hepatocellular carcinoma cells, promoted the apoptosis of hepatocellular carcinoma cells, and showed a good anti-tumor effect in animals.
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Research progress of haptoglobin in digestive system tumors

He Chao, Yang Chun Bai Xue, Zhang Hao, Diao Qingfei, Jia Juming, wuxueliang, Fan Jianchun

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Gastrointestinal tumors pose a serious threat to human health, with their incidence and mortality rates accounting for more than half of all malignant tumors. Haptoglobin (Hp), an acute-phase glycoprotein, has been found to be elevated in both plasma and tumor tissues in various clinical conditions, particularly in different types of cancers such as liver cancer, gastric cancer, colorectal cancer, pancreatic cancer, and gallbladder cancer. Numerous studies suggest that Hp plays a significant role in the prognosis of cancer patients, highlighting its potential as a prognostic marker for gastrointestinal tumors with important clinical applications. Although research indicates that Hp is crucial in the development of various tumors, its specific mechanisms of action in gastrointestinal tumors remain controversial. Therefore, this paper reviews the differential expression and clinical significance of Hp in the five major types of gastrointestinal tumors, exploring its role in different stages of cancer progression and clinical prognosis. This aims to provide reliable and accurate serum biomarkers for the screening, early diagnosis, treatment, and prognosis monitoring of gastrointestinal tumors, which is of great significance for predicting the survival and prognosis of cancer patients.
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Role of Cancer-Associated Fibroblasts in the Formation of the Pre-Metastatic Niche

Ziting Wang1, Guantong Yang1, Jianchun Fan2, Siqi Gao1, Rui Guo1, Lina Jiang1, Yaxiong Guo1

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As the global incidence of cancer continues to rise, tumor metastasis has emerged as the leading cause of death among cancer patients. The formation of the pre-metastatic niche creates a favorable microenvironment for tumor cell colonization and metastasis, significantly driving the spread of cancer. In this context, cancer-associated fibroblasts (CAFs) have garnered significant attention for their multifaceted roles in tumor progression. CAFs contribute to the establishment of the pre-metastatic niche and enhance the invasive behavior of tumor cells by remodeling the extracellular matrix, inducing epithelial-mesenchymal transition, stimulating angiogenesis, and modulating the tumor immune microenvironment. These actions not only accelerate the metastatic process but also facilitate immune evasion by the tumor. This review delves into the pivotal mechanisms and functions of CAFs in tumor metastasis, exploring their potential applications in cancer research and therapy, and offering new perspectives for the development of anti-metastatic strategies.
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Research progress of SHP2 in colitis associated colon cancer and colorectal cancer

wuxueliang

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【】Colorectal cancer (CRC), as one of the most common malignant tumors that threaten human life, seriously affects the quality of life of patients. In recent years, SHP2 has become a hot topic in the field of cancer and has been proven to have a close relationship with colorectal cancer. SHP2, Encoded by the PTPN11 gene, it is a non receptor tyrosine kinase commonly present in various tissues and cells of the human body. Existing research shows that, SHP2 plays a crucial role in regulating CRC and colitis associated colon cancer (CAC). And with the emergence of SHP2 allosteric inhibitors, SHP2 has become a new potential therapeutic target for CRC patients. This article mainly reviews the structure of SHP2 and its impact in CRC and CAC.
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Research Progress on Animal Models of Lung "Inflammation-Cancer" Transformation

chen yajuan, chen lanying, duan wenbin, huang yuqing, jin xuhui

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[Abstract] Lung cancer is a serious pulmonary tumor disease, and the exacerbation of its chronic inflammatory state is a precursor to lung cancer formation. To gain a deeper understanding of the pathogenesis of lung cancer and to develop preventive treatment strategies, relevant animal models are widely used in experimental research. In particular, induced lung cancer animal models are considered an important entry point for understanding the transition from chronic lung inflammation to lung cancer. Early intervention is of great significance for the prevention and treatment of lung cancer. Based on this, this paper reviews recent literature on various inducing factors of lung cancer, including many carcinogens (such as Nicotine-derived nitrosamine ketone(NNK), B[a]P, Benzopyrene(DEN), Atmospheric fine particulate matter(PM2.5), coal smoke, heavy metal ions, radiation, biological infections, etc.). It summarizes the animal models of lung inflammation and cancer transformation induced by these factors, discusses the mechanisms by which relevant carcinogens induce lung cancer, analyzes the advantages and limitations of animal models, and looks forward to future development directions. The aim is to provide a valuable reference for the establishment of related models in the future.
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Progress in the animal model of pollen-induced allergic rhinitis

XuDan, GaoFeihong, LiLin, LiShanshan, WangYili

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【Abstract】Pollen allergen-induced allergic rhinitis (AR), also known as seasonal allergic rhinitis (SAR), typically manifests during the pollen dissemination period of anemophilous plants. Over the past three decades, the prevalence of SAR has more than doubled. The etiology of SAR is multifaceted, encompassing various elements such as pollen allergens, environmental and climatic conditions, genetic predispositions, and the immunological status of individuals.Animal models serve as a critical tool in elucidating the mechanisms underlying AR and in advancing the development of efficacious preventive and therapeutic strategies. This review synthesizes the pertinent literature on pollen-sensitized AR animal experiments conducted both domestically and internationally over recent years. It systematically delineates the factors influencing the efficacy of these models, including the selection of animal strains, the production and associated challenges of sensitizing agents, specifically pollen antigens, the utilization and limitations of adjuvants, the procedural steps involved in model creation, and the methodologies for evaluating model effectiveness.The insights provided herein are intended to offer guidance and support for the development of appropriate animal models of pollen-induced AR, thereby facilitating both fundamental and applied research in this area.
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Research progress of berberine in neuroprotection of Parkinson"s disease

lihongyu, lanrui, tangchen, liushuang, zhangyong, shenxiaoming

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Parkinson"s disease (PD) is a neurodegenerative disease commonly found in middle-aged and elderly people. A type of disease characterized by static tremors, bradykinesia, muscle rigidity, and postural balance disorders in clinical practice. Berberine (BBR) is a natural quinoline alkaloid. In recent years, studies have found that berberine has hypoglycemic, lipid-lowering, antioxidant, and anti-inflammatory effects, and can effectively improve the misfolding and aggregation of alpha synuclein. Its mechanism of action may include reducing inflammation, alleviating oxidative stress, improving mitochondrial autophagy, regulating intestinal microbiota, and clearing function. This article systematically reviews the mechanism of action and research status of berberine in the neuroprotective field of Parkinson"s disease, providing some reference for the future clinical application and treatment of berberine in Parkinson"s disease.
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Study on the Role of DNA Methyltransferases in Neuroprotection During Hypoxia/Ischemia Preconditioning DNALI Ruixue1,XIE Yabin1,SHAO Guo1,2.

li rui xue, Xie Yabin, Shao Guo

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Hypoxic preconditioning can induce endogenous protective mechanisms that increase the tolerance of nerve cells to hypoxia/ischemia. This protective mechanism involves changes in gene expression during the critical decision-making period between cell survival and death. DNA methylation, as a crucial mechanism for gene expression regulation, plays an essential role in hypoxia/ischemia tolerance. DNA methyltransferases (DNMTs) contribute to neuroprotection by influencing gene expression through the regulation of DNA methylation levels. Therefore, DNMTs have significant functions in the neuroprotection induced by hypoxic/ischemic preconditioning. This paper reviews the role of DNMTs in this process, providing insights into neuroprotection targeting DNMTs.
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Research Progress on the Mechanism of MicroRNA Regulation in IBS-D and Intervention with Traditional Chinese Medicine

hechanghui, panhaidi, douxin, meixiao, wangwei

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The incidence of diarrhea-predominant irritable bowel syndrome (IBS-D) remains high, with microRNA-mediated intestinal barrier dysfunction, visceral hypersensitivity, low-grade inflammation, and dysbiosis playing significant roles in its pathogenesis. Studies found that traditional Chinese medicine can treat IBS-D by directly or indirectly targeting miRNA to regulate multiple pathways and targets in a coordinated manner. This article systematically reviews the involvement of miRNA in the pathogenesis of IBS-D and the progress of traditional Chinese medicine interventions. It explores the relationship between traditional genetics, epigenetics, and the Chinese medicine concepts of "kidney" and "spleen" in terms of congenital and acquired interactions from a molecular biology perspective. This provides a reference for exploring the micro-material basis of traditional Chinese medicine's Zang-Xiang theory and offers new ideas and methods for the effective treatment of IBS-D with traditional Chinese medicine.
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Exploration and practice of the elective course “Practical Mouse Anatomy & Comparative Medicine” in undergraduate stage under the perspective of teaching and research integration

YANGQIAO, CAO GANG

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The elective course “Practical Mouse Anatomy & Comparative Medicine” is a comprehensive technical course designed to cultivate the foundational theoretical knowledge and experimental skills in laboratory mouse anatomy for undergraduate students in medical and pharmaceutical-related fields. With the increasing demand for innovation and entrepreneurship training programs and undergraduate participation in research laboratories, this course systematically teaches the anatomical knowledge of the eight major systems and local anatomy of experimental mice, emphasizing the combination of theory and practice to provide a comprehensive learning platform. The course continually explores and reforms its practices to ensure that the teaching content keeps pace with the forefront of scientific research, fostering a rigorous and pragmatic scientific attitude in students, thereby laying a solid foundation for their future research work. This paper discusses the effectiveness of the course in enhancing students’ research literacy and practical abilities, aiming to provide a reference for the design and implementation of similar courses.
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Mechanistic study of miR-207 regulates Mycobacterium tuberculosis survival in macrophages

DU Wenya, DAI Yumei, YUE Linzhi, MA Tao, WU Lixian

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【Abstract】Objective miR-207 is differentially expressed in many diseases. It investigate the mechanism study of miR-207 overexpression on regulating the survival of Mycobacterium tuberculosis (H37Ra) in macrophages to provide a theoretical basis for targeted therapy of tuberculosis. Methods The experiment was divided into four groups: blank group (Ana-1 cells only), control group (cells infected with H37Ra), mi group (infected with H37Ra and transfected with miRNA-207 mimics), and mi-NC group (infected with H37Ra and transfected with mimics NC). A model of TB infection was established using H37Ra infected Ana-1 cells, and miRNA-207 mimics and mimics NC were transfected into Ana-1 cells using the liposome transfection method. Tuberculosis colony-forming unit counting to assess the effect of miR-207 on intracellular mycobacterial load and clearance of extracellular residual mycobacteria. Flow cytometry was used to detect the total apoptosis rate. The relative expression of miR-207, apoptosis genes, pyroptosis genes, inflammation genes and autophagy genes were measured by qRT-PCR. western blot was used to detect the relative expression of apoptosis proteins, pyroptosis proteins and autophagy proteins. Fluorescence microscope and multifunctional enzyme labeling instrument were used to detect the fluorescence intensity of intracellular ROS, as well as to detect the content of intracellular LDH. Results Successful establishment of infection model was observed under the microscope. qRT-PCR detection found that miR-207 expression in control group was lower than that in blank group, indicating that miR-207 was differentially expressed in blank and control groups. miR-207 expression in mi group was significantly higher than that in mi-NC group, indicating successful establishment of transfection model. Colony forming unit counting found that the number of colonies in the mi group was higher than that in the mi-NC and control groups. The total apoptosis in mi group was higher than that in mi-NC and control groups by flow cytometry. qRT-PCR and western blot showed that the relative expression of apoptotic genes and apoptotic proteins was higher than that in blank group in control group, and that in mi group was higher than that in mi-NC group. the relative expression of inflammatory genes was higher than that in blank group in control group, and the relative expression of inflammatory genes was higher than that in mi-NC group, and the relative expression of inflammatory genes was higher than that in mi-NC group. The relative expression of inflammatory genes in control group was higher than that in blank group, and that in mi group was higher than that in mi-NC group, and the relative expression of pyroptosis genes and pyroptosis proteins in control group was higher than that in blank group and that in mi group was higher than that in mi-NC group. The relative expression of autophagy positively regulated genes LC3 and Beclin1 as detected by qRT-PCR was higher in the control group than in the blank group, and lower in the mi group than in the mi-NC group. The relative expression of negatively regulated autophagy genes had the opposite trend to that of autophagy positively regulated genes. The relative expression of autophagy-related proteins was consistent with the trend of autophagy genes. ROS fluorescence intensity was found to be higher in control group than in blank group, and higher in mi group than in mi-NC group. LDH content was found to be higher in control group than in blank group, and there was no statistically significant difference between the content in mi group and that in mi-NC group.The relative expression of negatively regulated autophagy genes LC3 and Beclin1 was higher than that in blank group, and lower than that in mi-NC group. Conclusions The miR-207 overexpression promotes apoptosis, cellular pyroptosis and inflammation, inhibits autophagy, favors H37Ra survival and provides a new direction for the treatment of tuberculosis.
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Xuanfei Jiedu Formula improves lung injury in rats with multidrug-resistant Pseudomonas aeruginosa pneumonia by inhibiting IKK/NF-κB signaling pathway

HAN Bing Yang, Shen Tingting, Fan Zhengyuan, Li Gaofeng, Li Ya, Li Suyun

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[ Abstract ] Objective To investigate the operational dynamics through which the Xuanfei Jiedu Formula ameliorates pulmonary damage in rats afflicted with Multidrug Resistant Pseudomonas Aeruginosa (MDR-PA) pneumonia, by modulating the activity of the IKK/NF-κB signal transduction cascade. Methods Eighty-four rats were randomly divided into 7 groups : Control group, Model group, XFJDF-low dose group, XFJDF-medium dose group, XFJDF-high dose group, Imipenem ( IPM ) group and Pyrrolidinedithiocarbamate ammonium ( PDTC ) group. 12 in each group. The MDR-PA pneumonia rat model was established by oral tracheal intubation. After the model was successfully constructed, the rats in the low, medium and high dose Xuanfei Jiedu Decoction groups were given the corresponding dose of drugs by gavage, the rats in the imipenem cilastatin group were given intraperitoneal injection of IPM, while the rats in the control group and the model group were given the same volume of normal saline by gavage, twice a day for 7 days. PDTC was intraperitoneally injected at 1 h before model establishment, 12 h and 24 h after model establishment in NF-κB inhibitor group. The behavior status, body weight change, spleen and thymus index, lung wet weight / lung dry weight ratio of rats were observed. The pathological changes of lung tissue were evaluated by HE staining. TUNEL staining was used to detect the apoptosis of lung tissue cells. The levels of IL-1β, TNF-α, TGF-β and IL-10 in serum were detected by ELISA. The contents of GSH and MDA, MPO activity and total antioxidant capacity ( T-AOC ) in serum of rats were determined by colorimetry and TBA method. The expression of NF-κBp65 in lung tissue was detected by immunohistochemistry. The expression of IKKβ and NF-κBp65 mRNA in lung tissue was analyzed by PCR. The expression levels of IKKβ, p-IKKβ, NF-κBp65 and p-NF-κBp65 in lung tissue were measured by Western Blot. Results Compared with the Control group, the rats in the Model group had reduced diet, lack of luster in hair, slow response, reduced activity, accelerated respiratory rate, accompanied by murmurs, and significantly reduced body weight ( P < 0.01 ). Marked enhancements were observed in both the spleen and thymus indices (P < 0.01). The lung wet weight / lung dry weight ratio exhibited a substantial rise (P < 0.01), concurrently with an augmentation of alveolar secretions in lung tissue. Infiltration of abundant inflammatory cells was noted, alongside a notable escalation in lung tissue apoptosis. Serum concentrations of IL-1β, TNF-α, TGF-β, and IL-10 demonstrated a substantial upsurge (P < 0.01), alongside an augmented MDA content and heightened MPO activity (P < 0.01). Conversely, GSH levels and T-AOC capabilities displayed a notable decline (P < 0.01). In the lung tissue, there was a remarkable elevation in the expression of IKKβ and NF-κB p65 mRNA (P < 0.01). Furthermore, the ratios of p-IKKβ/IKKβ and p-NF-κBp65/NF-κBp65 in the lung tissue also showed a significant rise (P < 0.01).Compared with the Model group, the treatment group could improve the above indicators to varying degrees ( P < 0.05, P < 0.01 ), among which the Xuanfei Jiedu Formula high-dose group and the IPM group were more significant. Conclusion Xuanfei Jiedu Formula may improve lung injury in rats with MDR-PA pneumonia by inhibiting IKK / NF-κB signaling pathway.
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Protective effect and mechanism of Glycosides of cistanche on rats in cerebral ischemia reperfusion injury model

WANG Lu, GUO Xia, MA Shangjia, YONG Wen, YU Wenlong, WU Lie, JIA Jianxin

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Objective To investigate the neuroprotective effect of Glycosides of cistanche (GCs) on cerebral ischemia reperfusion injury in rats and its mechanism. Methods Forty-eight male Wistar rats were randomly divided into Sham group, Model group, GCs group and Nim group. A rat model of focal cerebral ischemia reperfusion injury (CIRI) was established by middle cerebral artery occlusion (MCAO). Sticker removal test, balance beam test, and open field test were used to evaluate the sensory and motor abilities of rats in each group. TTC staining was used to detect the area of cerebral infarction, Nissl staining was used to observe the morphology of nerve cells, and TUNEL staining was used to detect the apoptosis of nerve cells. The expressions of apoptosis-related proteins Bax, Bcl-2 and Caspase-3 were detected by immunohistochemical staining and Western blot. Results Compared with the Sham group, the neurological deficit score was significantly increased (P < 0.05), the time of removing stickers and passing balance beam was significantly increased (P < 0.01), the motor ability was decreased, the infarct size was increased, the number of neurons was decreased, and the number of apoptotic cells was increased after cerebral ischemia reperfusion. The expressions of Bax and Caspase-3 were significantly increased (P < 0.05), and the expression of Bcl-2/Bax was significantly decreased (P < 0.05). Compared with the Model group, GCs could improve the behavioral performance of cerebral ischemia reperfusion model rats, reduce the infarct size, inhibit cell apoptosis, down-regulate the expression of Bax and Caspase-3 (P < 0.05), and up-regulate the expression of Bcl-2/Bax (P < 0.05). Conclusion GCs has a neuroprotective effect on cerebral ischemia-reperfusion injury, which may play a role in inhibiting cell apoptosis by regulating the expression of apoptosis-related factors Bax, Bcl-2 and Caspase-3.
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Regulation of Nrf2 on activation and polarization of microglia induced by Methamphetamine

YANG Genmeng, PENG Yanxia, ZHANG Xinjie, HOU Yuhan, XU Jing, LI Lihua, DU Qi, HONG Shijun

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Objective To investigate the regulation of Nrf2 on activation and polarization of microglia induced by METH. Methods BV2 cells and HMC3 cells were studied in vitro. Wild-type mice and Nrf2 knockout mice were studied in vivo.TheStoxicity models induced by METH inSvivoSand inSvitro were established respectively. And the IF and WesternBlot were used to detect the activation and polarization of microglia in each group, respectively. Results After treatment with METH, the fluorescence level of iNOS(Marker protein of polarized M1 phenotype in microglia) increased significantly in BV2 and HMC3 cells, while the fluorescence level of Arg1 (Marker protein of polarized M2 phenotype in microglia) decreased significantly. The results showed that METH could induce microglia polarization, and enhance the pro-inflammatory effect, and reduce the anti-inflammatory effect of microglia. The Nrf2 gene knockout mice were used to further explore the regulation of Nrf2 on the activation and polarization of microglia induced by METH. The results showed that after exposure to METH, microglia in the cortex of mice were obviously activated, and the expression levels of IBA1 and iNOS were obviously increased, while the expression level of Arg1 was decreased. Compared with wild-type METH group, the number of microglia activated after Nrf2 gene knockout was significantly increased, while the expression levels of IBA1 and iNOS were increased and the expression level of Arg1 was decreased. The above results indicated that METH could enhance the pro-inflammatory effect of microglia and reduce its anti-inflammatory effect while inducing the activation and polarization of microglia. However, after Nrf2 gene was knocked out, the effect of METH activated microglia and its pro-inflammatory and anti-inflammatory effects were stronger. Conclusions Nrf2 plays an important role in regulating the activation and polarization of microglia induced by METH, and Nrf2 was expected to be a potential target for the treatment of neuroinflammation induced by METH.
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Research progress of exosomal miRNAs in methamphetamine-induced neurotoxicity and drug development

ZHOU Ying, SUN Wei, YANG Genmeng, DONG Wenjuan, HONG Shijun, LI Lihua

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As a new type of abused drug, methamphetamine (METH) has a strong central stimulant effect, and the excitatory pathway involved a series of central higher-level functions, including drug-related rewards and motivation, learning and memory, decision-making and execution, etc. Methamphetamine not only causes neurotoxicity in the body, but long-term use could cause cognitive dysfunction, loss of personality, and serious social violence in addictions. Exosomes, as a new carrier of cell-to-cell communication, were involved in the occurrence and development of drug addiction, and exosome miRNAs were not only important biomarkers for methamphetamine addiction, but also involved in various aspects of methamphetamine induced neurotoxicity, which could be used as a therapeutic carrier to provide new ideas for the diagnosis and treatment of methamphetamine abuse.
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Application of gene-editing technique in experimental animals

LIU Chaonan, YAN Lihong, WANG Jing, SHEN Yanhua, PAN Mingming, ZHOU Zhengyu

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Recently , with the rapidly developing of molecular biological technique, gene-editing, as a means of genome modification, has been used in the establishment of experimental animal models due to its high efficiency, accuracy and flexibility. This article mainly summarizes the construction and application of the latest gene-editing technique in animal models such as experimental animal pigs, non-human primate, and experimental animal dogs, it provides a theoretical reference for the applied widely and in-depth study of gene-editing technique in experimental large animals, so as to better simulating human diseases and study the potential pathogenesis of biomedical and human complex diseases.
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Research progress of autophagy in pathogenesis of idiopathic pulmonary fibrosis

DU Weifei, LIU Xiaoming

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Autophagy, as a crucial physiological process of cells, is an important mechanism to maintain cell homeostasis and regulate cell survival. idiopathic pulmonary fibrosis (IPF), as an interstitial lung disease with unknown etiology and poor prognosis, is characterized by alveolar epithelial cell damage, abnormal proliferation and activation of fibroblasts. It is accompanied by the excessive deposition of extracellular matrix (ECM). Its pathogenesis involves a complex interaction between cell types and signaling pathways. Studies have shown that defects in autophagy function play a key role in the occurrence and development of pulmonary fibrosis. This review aims to investigate the mechanism of autophagy in IPF and reveal its complexity and related signaling pathways.
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Relationship Between Color Doppler Ultrasound Parameters and Insulin Sensitivity Index and Clinical Efficacy in Rats with Polycystic Ovary Syndrome Complicated with Hyperinsulinemia

Sun Xizhen, Geng Linlin, Zhang wei, Chen juan, Sun Deming, Li Nan

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Objective To analyze the relationship between color doppler ultrasound parameters and insulin sensitivity index (ISI) and clinical efficacy in rats with polycystic ovary syndrome (PCOS) combined with hyperinsulinemia (HI). Methods 140 3-week-old female SD rats of SPF grade were selected and randomly divided into two groups. The PCOS combined with hi rat model (Study Group) and PCOS without hi rat model (control group) was prepared respectively. After successful modeling, the rats were examined by color doppler ultrasound, and the total area (TA), ovarian volume (OV), interstitial area (SA), vascularization index (VI), blood flow index (FI), vascularized blood flow index (VFI), peak systolic blood flow velocity (PSV), peak diastolic blood flow velocity (PDV), resistance index (RI), and ovarian interstitial artery pulsation index (PI) were compared between the two groups. Fasting insulin (fins) and fasting blood glucose (FPG) were measured in rats" fasting venous blood at the same time, and ISI was calculated. Pearson correlation analysis was used to analyze the correlation between color doppler ultrasound parameters and ISI in the study group. The rats in the study group were treated with metformin by intragastric administration. According to the therapeutic effect, the rats in the study group were divided into the good effect group and the poor effect group. The color doppler ultrasound parameters of the two groups were compared, and the receiver operating characteristic curve (ROC) was drawn to analyze the value of color doppler ultrasound parameters in evaluating the curative effect of PCOS combined with hi rats. Results: 65 rats with PCOS and hi were successfully established in the study group, and 60 rats without PCOS and hi were successfully established in the control group. The body weight, body mass index, systolic blood pressure, diastolic blood pressure, Ta, OV, SA, VI, fi, VFI, PSV, PDV, fins and FPG of the study group were higher than those of the control group, while RI, PI and ISI of the study group were lower than those of the control group, and the differences were statistically significant (P<0.05). Pearson correlation analysis showed that color doppler ultrasound parameters TA and SA were negatively correlated with ISI (r=-0.501, -0.492, P<0.05), and ovarian RI and PI were positively correlated with ISI (r=0.504, 0.485, P<0.05). In the group with good curative effect, Ta、OV、SA、VI、FI、VFI、PSV、PDV、 Low density lipoprotein cholesterol, FPG, fins, LH, FSH were lower than those in the poor efficacy group, RI, PI were higher than those in the poor efficacy group, the difference was statistically significant (P<0.05). ROC curve analysis showed that the sensitivity and specificity of color doppler ultrasound parameters combined with clinical efficacy were 90.9% and 90.2%, respectively, and the area under the curve (AUC) was 0.901. Conclusion Color doppler ultrasound parameters are closely related to ISI and clinical efficacy of PCOS combined with hi rats, which can predict the clinical efficacy of such patients to a certain extent.
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Research advances in the regulation of HPA/HPT/HPG axis in the treatment of depression in traditional Chinese medicine

li chao, wang meng

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The pathogenesis of depression is complex and the treatment methods are limited, and it is of great significance to clarify its pathogenesis and develop new therapeutic drugs. Currently, hormones and hormone-modifying compounds have been used to treat depression, and their therapeutic effects are attributed not only to the regulation of the peripheral endocrine system, but also to the effects of hormones on the central nervous system of non-endocrine brain circuits. HPA/HPT/HPG is closely related to the pathogenesis of depression. The mechanism of action of traditional Chinese medicine in the treatment of depression is extensive, and the regulation of the three axes also presents a variety of ways. Based on the new evidence of hormones and hormone operon compounds involved in the pathology and treatment of depression, this paper summarizes the relevant mechanisms of current traditional Chinese medicine in the treatment of depression, in order to provide ideas and references for the research of traditional Chinese medicine.
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The effect of Creb expression in the prefrontal cortex on depressive behavior in rats

Liugaoyuan, Pengmengwei, Luozilong, Kuoluoyi, Chenyulong, Yangtiezhu, Wuyaosong, Liuyan

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Objective To observe the influence of Creb protein over-expression and under-expression in the prefrontal cortex on depressive behavior in rats. Methods Adeno-associated virus (AAV) strains that can knock down Creb expression in the prefrontal cortex of rats were injected by using stereotaxic injection method and screened by using Western blot, qRT-PCR and immunofluorescence methods. 40 Rats were randomly divided into control group（Control）,chronic restraint stress group（CRS）,chronic restraint stress combined with adeno-associated virus interference group（CRS＋AAVI）and chronic restraint stress combined with adeno-associated virus overexpression group（CRS＋AAVO）. During the establishment of animal model, the body weight and food intake of each group of rats were monitored. After the establishment of the animal model, the behavioral changes of rats were monitored by using sucrose preference test, elevated plus maze test, forced swimming test and open field test. The contents of 5-hydroxytryptamine (5-HT), norepinephrine (NE) and corticosterone (CORT) in the prefrontal cortex of rats in each group were measured by using Elisa method. Results The results of Western blot and immunofluorescence detection showed that the expression of Creb protein of rats in shRNA2 group was significantly lower than that of the other groups (P< 0.05). The results of qRT-PCR experiment showed that the expression of Creb mRNA in the shRNA2 group was significantly lower than that of the other three groups. Therefore, the AAV-Creb1-shRNA2 virus strain was selected for modelling of subsequent Creb knock-down experiments in this study. After knock down and high expression Creb AAVs were injected into the brains of rats, compared with other groups, the food intake of rats in the CRS＋AAVI group was significantly reduced compared with other groups (P< 0.05). At the same time, the rats in this group showed slow weight gain, decreased desire and pleasure to explore new environment, significantly increased despair and nervous behavior, significantly decreased 5-HT and NE levels in the prefrontal cortex, and significantly increased CORT levels. While these depressive behaviors and associated neurotransmitter levels were reversed by injection of the overexpressing AAV-Creb1 virus strain. Conclusion Lower expression of Creb in the prefrontal cortex can aggravate the degree of depression in rats, while the high expression of Creb can alleviate the degree of depression of rats to a certain extent. These results further confirm that Creb expression in the prefrontal cortex is one of the important targets involved in the pathogenesis of depression, and can provide ideas and references for the construction of animal gene models and pathogenesis of depression in future.
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Evaluation study on zebrafish insomnia model by illumination method and combined illumination and caffeine method

san yuqing

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【】 Objective: to establish different sleep deprivation models using zebrafish to provide more reproducible and practical modeling reference solutions for basic research on insomnia. Methods: Zebrafish insomnia model was induced by two interventions: continuous light (150 lux) and light plus caffeine, and the zebrafish were randomly divided into control, light, combined and caffeine (100 μmol/l) groups. The difference in locomotor ability of zebrafish in each group was observed by using open field experiment and circadian rhythm behavioral experiment; the expression and secretion of related sleep genes and 5-HT neurotransmitter were detected by using Qpcr technology and Elisa technology. Results: 1. The sleep time of zebrafish in the light group was significantly reduced compared with that of the blank control group (P=0.01), and there was no statistically significant difference between the sleep time of zebrafish in the combined group and the caffeine group (see Table 1); the resting time of zebrafish during the daytime in the light group was significantly reduced compared with that of the blank control group (P<0.01), and the resting time during the daytime of zebrafish in the combined group and the caffeine group was increased (P<0.01) (Table 3). There was no statistically significant difference in the black light resting time of zebrafish in all groups (Table 3); the daytime moving distance of zebrafish in the light group was significantly increased compared with that of blank control group (P < 0.01), and the 10-h activity distance of zebrafish in the light group in the dark day was significantly increased compared with that of blank control group (P < 0.01), and there was no statistically significant difference in the dark day activity distance of zebrafish in the combined and caffeine groups (Table 4); and the sleep rounds of zebrafish in the light group was blank control group was significantly reduced (P < 0.01), and the sleep rounds of zebrafish in the combined and caffeine groups were significantly increased (P < 0.01) compared to the blank control group (Table 2).2. The percentage of swimming distance in the central region of the light group was reduced (P < 0.05) compared to the blank group, while the percentage of swimming distance in the central region of the caffeine group was significantly reduced (P < 0.01) compared to the light group (see Figure 6); the light group The percentage of swimming time in the central region was lower than that in the blank group (P < 0.05), while the percentage of swimming time in the central region was significantly lower in the caffeine group than that in the light group (P < 0.01) (Fig. 7).3. The expression of HTR1aa mRNA level in zebrafish in the light group was higher than that in the blank group at 6:00 a.m. and 12:00 p.m. (P < 0.05) (Figs. 10 and 11), and the expression of There was no statistically significant difference in the expression of HTR1ab mRNA levels between the light group and the combined group (P > 0.05) (Figs. 12 and 13); compared with the blank group, the amount of 5-HT secretion in the light group was reduced in both groups at 6:00 a.m. (P < 0.01), and at 12:00 p.m. the amount of 5-HT was reduced in both the light and combined groups (P < 0.01), and the amount in both groups remained lower than that in the blank group at 6:00 p.m. (P<0.01).
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The effects of combined exposure to PM2.5 and high-salt diet on liver inflammatory cytokines and lymphangiogenesis in mice

ding shibin, JIANG Jinjin, LI Yang

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Objective The effects of combined exposure to PM2.5 and high-salt diet on hepatic inflammation and lymphangiogenesis in mice. Methods Thirty-two C57BL/6J mice were randomly assigned to: control group, PM2.5 group, high-salt group and PM2.5+high-salt group. Mice in the high-salt group and PM2.5+high-salt group were fed with 8% high-salt diet for 8 weeks, mice in the other groups were fed with control diet containing 0.4% salt. Mice in the PM2.5 group and PM2.5+high-salt group were treated with PM2.5 by tracheal instillation (twice per week); and mice in the mice in the other groups were instilled with equal volume of saline at the same time (twice per week). All mice were sacrificed after the last PM2.5 exposure. TNF-α and IL-6 in liver tissues of mice were determined. Moreover, the LYVE1 expression of liver tissues were?visualized using immunofluorescence staining. The protein expression levels of lymphangiogenesis markers PROX1 and LYVE1, lymphangiogenesis regulatory proteins VEGFR-3 and VEGF-C in liver tissue were measured using Western blot. Results Compared to the control group, the levels of TNF-α and IL-6, as well as the protein expressions of PROX1，LYVE1, VEGFR-3 and VEGF-C in liver tissues of mice in the high-salt group (HSD) were obviously increased (P<0.05). Compared to the HSD, the levels of TNF-α and IL-6 and the protein expressions of PROX1，LYVE1, VEGFR-3 and VEGF-C in liver tissues of mice in the PM2.5+HSD were obviously increased (P<0.05). Moreover, there were significant interaction effects between PM2.5 and high-salt diet on these above indicators. Conclusions Combined exposure of PM2.5 and high-salt diet obviously aggravated hepatic inflammation, and may increase hepatic lymphangiogenesis through upregulating VEGFR-3 and VEGF-C in the liver of mice.
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The application value of dual energy CT imaging in the evaluation of bone repair

sudanyang, mayuanbo, liujinlong, zhanghaoran, yangshenyu, miaoqiuju, baizhen, yangxiaopeng

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Bone defect repair is an urgent problem to be solved in the field of orthopedics, and numerous researchers are working to develop more effective treatment plans. However, accurate evaluation of bone repair after surgery is an crucial step. With the development of computed tomography (CT) imaging, dual energy CT imaging has shown significant advantages in analyzing bone composition and reducing metal artifacts. This article reviews the application value of dual energy CT imaging in the evaluation of bone repair in animals.
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MiRNA investigation of the regulatory effects of Allium guajava and Allium cepa sempervirens soup on the Epsin1-FGFR1 pathway in atherosclerotic mice

wang zhao bo, pan yi, lin qian

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: This study aimed to evaluate the therapeutic effects of Gualou Xiebai Banxia Decoction (GXBD) on atherosclerosis (AS) in a mouse model and to explore its underlying mechanisms. Male APOE-/- mice were used to induce the AS model through a 16-week high-fat diet. The mice were randomly divided into a model group, a control group, different dosage groups of GXBD, and a lipid-lowering drug group. Histological analysis using HE and Oil Red O staining was performed to observe changes in arterial walls and plaque formation. The results demonstrated that GXBD significantly reduced plaque formation. Further miRNA sequencing analysis revealed that GXBD regulated multiple AS-related miRNA genes, influencing the expression of key proteins such as Epsin1 and FGFR1, thereby exerting potential therapeutic effects on AS lesions. Western blot and immunofluorescence experiments further validated these regulatory effects. The findings suggest that GXBD exhibits significant efficacy in the treatment of atherosclerosis, potentially through miRNA regulation and protein expression modulation.
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Effects of RSPO2 on oxidative stress and apoptosis of ovarian granulosa cells

LI Shuo, LI Nian, ZHOU Xiaofeng, YUAN Xiaolong

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Objective Utilizing human ovarian granulosa tumor cells as the cellular model, we tried to investigate the effect of roofplate-specific spondin 2 (RSPO2) on the oxidative stress and apoptosis level of ovarian granulosa cells. Methods We performed transient transfection of RSPO2 overexpression plasmid and small interfering RNA (siRNA) in COV434 cells. Real-time Quantitative PCR (RT-PCR) and Western blot were used to detect efficiency of overexpression and interference. The reactive oxygen species assay kit was used to determine the amount of intracellular reactive oxygen species. The apoptosis level was detected by flow cytometry. RT-PCR and Western blot were used to determine the expression levels of oxidative stress and apoptosis-related genes. Co-immunoprecipitation was used to detect interacting proteins. Results The overexpression and interference of RSPO2 were successfully realized. Overexpression of RSPO2 significantly inhibited the level of reactive oxygen species in COV434 cells (P < 0.05) and extremely significant inhibited the early apoptosis of granulosa cells (P < 0.01), interference of RSPO2 obtained the opposite results. Overexpression of RSPO2 significantly upregulated the mRNA and protein levels of SOD1, SOD2, CAT (P < 0.05), and significant downregulated the levels of caspase 3 and caspase 8 (P < 0.05). On the contrary, interference of RSPO2 significantly downregulated the levels of SOD1 and CAT (P < 0.05), and significantly upregulated the level of caspase 3 and caspase 8 (P < 0.05). We found the protein interactions between RSPO2, SOD1, CAT and caspase 3. Conclusion Interfering with RSPO2 promotes the accumulation of reactive oxygen species within cells, downregulates the expression of SOD1 and CAT, thereby enhancing oxidative stress. Additionally, interfering with RSPO2 upregulates the expression of caspase 3 and caspase 8, promoting cell apoptosis. These findings suggest that RSPO2 plays a crucial role in ovarian granulosa cells.
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Current research status of ferroptosis in endometriosis

pengjiahua, song xin, liangruining, sun yu, jian hui, luoxiaoquan

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Endometriosis (EMs)? is a common challenge in global women"s health. In recent years, ferroptosis, as an emerging form of regulated cell death, has attracted attention in EMs research. In terms of disease mechanisms, ferroptosis drives ovarian EMs fibrosis through iron overload induction, and promotes disease progression by regulating multiple signaling pathways such as p38MAPK/STAT6, enhancing angiogenesis, autophagy, etc. In terms of infertility, ferroptosis affects embryo development and ovarian function, significantly reducing fertility. In terms of diagnosis, the high expression of ferroptosis-related genes provides potential biomarkers for early diagnosis of EMs, effectively distinguishing patients from healthy individuals, and has important clinical application value. In terms of treatment strategies, non-natural compounds like Erastin, as well as natural compounds like resveratrol, ursolic acid, baicalein, etc., show potential therapeutic effects, relieving the pathological process and related symptoms of EMs. Therefore, this article
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Research progress of the ketogenic diet in the field of Parkinson"s disease

LI Boyang, LAN Rui, YANG Huijie, LI Hongyu, LI Chiyang, SHEN Xiaoming

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A ketogenic diet refers to an eating pattern designed to promote individuals to achieve a low-calorie content, minimum carbohydrate intake, high-fat consumption, and standard protein levels. The ketogenic diet is used in clinical practice to treat applications including heart dis-ease, diabetes, obesity, autism, glioblastoma, and other cancers. However, the ketogenic diet has not been recommended for any neurological disorder except epilepsy. With the intensive research on the ketogenic diet in recent years, more and more evidence has proved that the ketogenic diet has a neuroprotective effect on Parkinson's disease, and it is a new dietary ther-apy for the treatment of Parkinson's disease. In this review, we discuss in detail the neuropro-tective effects of the ketogenic diet in Parkinson's disease by different mechanisms, aiming to provide some references for clinical and experimental studies in this field.
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Study on repairing effect of moxibustion at different acupoints

zhouhaiyi, hesiyi, hanruifang, guanyongge, donglijuan, Song Yang

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Objective: To compare the repair effects of moxibustion "Guanyuan" and "Shenshu" on thin endometrium rats. Methods: 32 SD rats were randomly divided into normal group, model group, Guan Yuan group and Shenshu group with 8 rats in each group. Thin endometrium model was established using 95% anhydrous alcohol. After two estrus cycles, the Guanyuan group and Shenshu group moxibusted "Guanyuan" and "Shenshu" points, once a day, and rested for 1 day every 6 days for a total of 21 days. The other two groups were fixed in the same way. The temperature changes in the acupoint area at different time were measured by infrared thermometer, the pathological morphology of uterus was observed by HE staining, and serum levels of IL-1β, IL-10, E2 and PROG were detected by ELISA. The expressions of Ki67, PCNA, LIF and ITG-β3 in uterus were detected by immunohistochemistry. The expression levels of ANG-1、CD34和VEGFA in uterus were detected by Western blot. Results: Immediately after moxibustion and 5min after moxibustion, the body surface temperature at Shenshu point was higher than that at Guanyuan point (P<0.001, P<0.01). Compared with normal group, endometrial thickness, number of glands and blood vessels in model group were decreased (P<0.0001, P< 0.01, P<0.001), The endometrial thickness, number of glands and blood vessels increased in Guanyuan group (P<0.0001, P<0.01, P<0.01) and Shenshu group (P < 0.0001, P<0.01, P<0.05),and the endometrial thickness, number of glands and blood vessels in Guanyuan group were better than those in Shenshu group, but the difference was not statistically significant. Compared with normal group, the serum IL-1β level in model group was increased (P<0.01), and the PROG level was decreased (P<0.001). Compared with model group, the serum IL-1β in Guanyuan group were decreased (P<0.01), E2 level and PROG level increased (P<0.01, P<0.05),and the serum IL-1β were decreased (P<0.05), IL-10,E2 and PROG levels (P<0.05, P<0.05, P<0.01) were increased in Shenshu group. Compared with normal group, the expressions of Ki67, PCNA, LIF and ITG-β3 of model group were decreased (P< 0.0001). Compared with model group, the expressions of Ki67, PCNA, LIF and ITG-β3 in Guanyuan group (P<0.0001) and Shenshu group (P<0.001, P<0.001, P<0.0001, P<0.001) were increased, and PCNA expression in Guanyuan group was higher than that in Shenshu group (P<0.05). The expressions of LIF and ITG-β3 in Shenshu group were stronger than those in Guanyuan group (P<0.01, P<0.05). Compared with normal group, the expression of ANG-1 and CD34 protein in uterine tissue of model group was decreased (P<0.0001). Compared with model group, the expressions of ANG-1, CD34 and VEGFA in Guanyuan group were increased (P<0.0001), and the expressions of CD34 and VEGFA in Shenyu group were increased (P<0.0001). The expression of ANG-1 in Guanyuan group was higher than that in Shenyu group (P<0.0001), while the expression of CD34 in Shenyu group was higher than that in Guanyuan group (P<0.05). Conclusion: Moxibustion "Guanyuan" point and "Shenshu" point could repair thin endometrium, Guanyuan point is superior to Shenshu point in reducing the level of inflammatory factors, increasing the level of E2, promoting the expression of proliferation factors, while Shenshu point is superior to Guanyuan point in increasing the level of anti-inflammatory factors and PROG, and promoting the expression of endometrium receptor related factors. The two points may play a role in promoting angiogenesis through different ways.
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Preliminary Study on the Application of Three-Dimensional Time-of-Flight Magnetic Resonance Angiography (3D-TOF-MRA) to Observe the Cerebral Arteries in Mongolian Gerbils

JIAO Kun, ZHANG Jing, MENG Xia, WANG Zhanjing, LEI Jianfeng, CHEN Baian, LU Jing

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Objective Establishment of a three dimensional time-of-flight magnetic resonance angiography (3D-TOF-MRA) technique for observing cerebral arteries in live Mongolian gerbils. Method 1. Employ a 7.0T MRI scanner to image the cerebral arteries of Mongolian gerbils, with data subsequently processed using the RadiAnt DICOM Viewer software；2. Validate and compare imaging results via the latex perfusion method；Attempt to perform 3D reconstruction of the posterior communicating branch and surrounding cerebral blood vessels of the Mongolian gerbil and rats through analysis software; 4. Attempt to use this method to screen individuals with abnormal vascular development in Mongolian gerbils to verify the effectiveness of this method. Result 1.The 3D-TOF-MRA technology can effectively observe the cerebral arteries of living Mongolian gerbils; 2.The 3D-TOF-MRA technology has high accuracy in observing the main cerebral arteries of Mongolian gerbils, but its observation effect on finer vascular branches is not as good as latex perfusion method; 3.The data obtained from 3D-TOF-MRA technology can be used for three-dimensional reconstruction of blood vessels; 4. The application of this technology has a good effect on screening for abnormal development of arterial structure in Mongolian gerbils. Conclusion The 3D-TOF-MRA technology can be applied to the structural observation and related research of the cerebral arteries in live Mongolian gerbils.
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Macrophage polarization in the research development of renal ischemia-reperfusion injury

SUN Haojie, LIU Xianqin, WANG Suogang ?

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Macrophages are important immune cells in innate immunity, with significant heterogeneity and polarization. It can polarize into various phenotypes (mainly M1 and M2) under the stimulation of various factors in the microenvironment, thus exerting different roles and functions. It plays an important role in the pathophysiological mechanism of renal ischemia-reperfusion injury (RIRI). Excessive immune response will inevitably lead to tissue damage. M1 macrophages are pro-inflammatory cells, which are involved in the clearance of pathogens. M2-type macrophages have anti-inflammatory effects and participate in the repair and remodeling of renal tissue after RIRI. The balance between macrophage phenotypes is important for the outcome and treatment of RIRI. Reason from the macrophage polarization Angle, the macrophages in RIRI pathophysiologic mechanism and the latest treatments, designed to further study the function of macrophage polarization in RIRI for reference, to adjust the macrophage polarization to improve RIRI treatment strategies.
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Research progress of TAM in tumorigenesis, development and drug resistance of gastric carcinoma

Cai Qiuling, Yang Jing, Shen Huiling, xuwenlin

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Tumor-associated macrophages(TAM) are a current focus in the study of the tumor microenvironment. To achieve their functionally distinct roles, macrophages undergo phenotypic polarizations resulting in two major subgroups: M1 macrophages with pro-inflammatory and anti-tumor effects, and M2 macrophages with anti-inflammatory and pro-tumor effects. Among them, M2 polarization, which is the main manifestation of TAM, has been associated with poor prognosis in various cancers and has shown supportive properties for malignancies. Gastric carcinoma patients have a low early diagnosis rate, late disease stage, and poor prognosis, with biological behavior characteristics of easy recurrence and metastasis. Currently, drug resistance and toxic side effects significantly limit the application and effectiveness of gastric carcinoma treatment. Therefore, it is urgent to explore new therapeutic drugs or targets. We summarize in this review the recent progress in the studies of TAM in the occurrence, development and drug resistance of gastric carcinoma, providing new ideas for clinical treatment and prognosis analysis of patients with gastric carcinoma.
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Construction of Lep gene knockout mouse model based on CRISPR/Cas9 system

CAO YUAN, YANG YUANSONG, GU WENDA, ZHAO HAOYANG, ZHAI SHIJIE, SUN XIAOWEI, FAN CHANGFA

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Objective The ob mice (C57BL/6-Lepem1/Nifdc) with the Lep gene knocked out mice (ob/ob) were generated by CRISPR/Cas9 system, establishing an animal model suitable for preclinical drug evaluation in clinical diseases such as diabetes. Methods According to the principle of CRISPR/Cas9 target design, sgRNA targeted mouse Lep gene was designed for transcription in vitro, and micoinjected with Cas9 mRNA into mouse zygotes. Mice tails DNA was extracted and detected by PCR and sequencing, followed by mating positive mice and wild-type mice. Blood biochemistry and liver pathology were assessed in homozygous ob mice. Results 8 positive mice were identified and a stable mouse strain was selected for further breeding. The serum triglycerides (TG), total cholesterol (CHO) and alanine aminotransferase (ALT) levels in homozygous ob mice were significantly higher than wild-type mice. Liver pathology result showed significant inflammatory infiltration and lipid vacuolar transformations. Conclusion The successful establishment of Lep gene knockout mice has enriched the national rodent experimental animal database and provided an animal model for preclinical drug evaluation.
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The role of astrocytes in traumatic brain injury and therapeutic strategies

Huang Yizhen, Cheng hao, Wang Hao-wei, Zhang Qian-yao, Luo Cheng-liang, Zeng Xiao-feng

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Traumatic brain injury (TBI) is an injury caused by the direct or indirect effects of external factors that result in structural or functional loss of brain tissue. Astrocytes, as homeostatic cells of the central nervous system, proliferate and activate rapidly in the early stages of TBI, and participate in a series of pathological processes such as neuroinflammation, blood-brain barrier disruption, glial scarring, and excitotoxicity after injury, and play a crucial role in the secondary neurological injury of TBI. This paper reviews the role of astrocytes in the repair of TBI damage with the aim of providing new strategies for the prevention and treatment of TBI.Traumatic brain injury (TBI) is a kind of craniocerebral injurious disease caused by external force that results in structural destruction of brain tissue and physiological dysfunction, with high morbidity, high disability, high mortality and high treatment burden, for which there has not yet been an effective therapeutic measure. Astrocytes, as homeostatic cells of the central nervous system, are rapidly proliferated and activated in the early stages of TBI to participate in a series of pathological processes such as neuroinflammation, blood-brain barrier disruption, glial scarring, excitotoxicity and other pathological processes after injury, and play a crucial role in the secondary neurological injury of TBI. The article focuses on the role of astrocytes in the pathological damage of TBI and reviews the research progress of astrocyte-targeted drugs, aiming to provide new strategies for the prevention and treatment of TBI.
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Research progress on anti-tumor effects of LRRC8A/VRAC ion channels

yangrunze, huyaohua, qinjing, wangyongfeng, shichanghong

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Volume adjusting anion channel (VRAC) in vertebrate cells and each type of general expression in tumor cells. Leucine-rich repeat containing 8A(LRRC8A) and its four homologous family members (LRRC8B-E), of which LRRC8A is an essential subunit. It has been confirmed that LRRC8A/VRAC is involved in the proliferation, migration, invasion and multi-drug resistance of tumor cells through various signaling pathways. This ion transporter has shown good potential in killing tumor cells and preventing the development of tumor, and can be used as a new target for tumor therapy. Therefore, this paper reviews the latest research on the involvement of LRRC8A/VRAC in tumorigenesis and development, including the molecular structure, function and regulation of LRRC8A/VRAC in tumor and immune cells, with emphasis on the application of LRRC8A/VRAC in tumor diagnosis and immunotherapy, in order to provide reference for exploring LRRC8A/VRAC as a new target of tumor therapy.
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The role of PI3K/AKT signal pathway in peripheral nerve injury and the research progress of traditional Chinese medicine intervention

guo xiaojing, ZHANG bo, Wang Yan, ZHANG Li

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Peripheral nerve injury (PNI), caused by contusions, fractures, and other traumas, leads to abnormal sensory functions, limited motor capabilities, neuropathic pain, and muscle atrophy, severely impacting patients' quality of life. Post-PNI, Wallerian degeneration occurs, involving axonal degeneration and myelin sheath collapse. Notably, the dorsal root ganglia (DRG), as the primary sensory neurons in pain signal transmission, are crucial targets in neuropathic pain (NP) induced by PNI. Therefore, changes in these targets trigger a series of complex signaling pathway alterations. Among them, the phosphatidylinositol 3-kinase/serine-threonine kinase (PI3K/AKT) signaling pathway, a vital regulator of cell survival and death, promotes Schwann cells (SCs) proliferation and migration, thereby enhancing axonal growth and myelination to facilitate nerve regeneration, and supports the survival of DRG neurons to alleviate NP. Current treatment methods include stem cell transplantation and neurotrophic medications, but all have certain limitations. Studies have shown that traditional Chinese medicine (TCM) has gained increasing attention and has been applied to some extent in the treatment of PNI due to its advantages of low cost and fewer side effects. This article discusses the relationship between oxidative stress, apoptosis, autophagy, inflammation, angiogenesis, the cell cycle, and other pathophysiological mechanisms in PNI and the PI3K/AKT signaling pathway, as well as its associated molecular targets. It also delves into the potential mechanisms of action of TCM monomers, compound formulas, and acupuncture based on the PI3K/AKT signaling pathway in the treatment of PNI, aiming to provide systematic and standardized theoretical guidance for the healing of PNI with TCM and a useful reference for the development of related medications.
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Research progress in the mechanism of PPARγ gene in osteoarthritis

Zhang Jian, Wang Dong, Qi Tiantian, Wu Liangbin, Yang Qi, Yu Fei

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Osteoarthritis (OA) is a chronic degenerative disease with a high incidence rate among middle-aged and elderly people. In the early stage, OA can be treated by conservative methods. In the late stage, most patients choose joint replacement and other surgical methods to treat OA, causing pain to patients and their families. Peroxisome proliferator activated receptor γ (PPAR γ) is a gene discovered in recent years that plays an important role in the degeneration or inflammation of OA cartilage, synovium, adipose, and other tissues. Signaling pathways such as AMPK, Wnt, and SIRT1 may be involved in this process. This review focuses on the role and mechanism of PPARγ gene’s function on OA via joint related tissues and signaling pathways.
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Biogenesis of exosomes and their role in neurodegenerative diseases

GuoSixu, MeiXinxin, LiJin

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The incidence of neurodegenerative diseases (NDs) is increasing with the years, and current drugs targeting NDs are basically symptom-based, not therapeutic, so they can’t prevent disease progress. Exosomes are a subset of extracellular vesicles that can be produced by all cells in the human body and exert biological effects in a variety of ways after they are released into the extracellular environment. Many studies have shown that although exosomes have two sides in the central nervous system, they can still be used as a tool for the prevention, remission, treatment and diagnosis of NDs due to their unique biological characteristics. This article reviews the biogenesis of exosomes and their roles in neurodegenerative diseases, so as to provide new ideas for clinical treatment of NDs.
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Research progress on hypoxic cell models

LI Jing, XU Dongyang, LI Changqing, SU Mengyao, WANG Zhijuan, ZHAO Mingjun, ZHAO Jialong, YANG Junyi, YANG Qiaodie, Kang Longli

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Hypoxia is associated with the occurrence and development of many diseases in clinical settings. Cell hypoxia not only serves as a vital marker for disease advancement but also plays a pivotal role in exacerbating the disease process. Therefore, improving tissue hypoxia may provide new strategies for the treatment of related diseases.. To investigate these diseases at the cellular and molecular levels, it is paramount to establish a cellular hypoxia model. At present, the extensively employed hypoxic cell models can be primarily categorized into three types: chemical hypoxia model, physical hypoxia model, and glucose deprivation hypoxia model.This article will overview the various types of hypoxic cell models and scrutinize their application and limitations in disease research.
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Vascular smooth muscle cell phenotype switch and Cell pyroptosis in the role and research progress of Abdominal aortic aneurysm

Liu Xin, Tang hongyue, Guo chang, Ma dong, Zhang mingming

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Abdominal aortic aneurysm (AAA) is a hidden and fatal disease, but its underlying developmental mechanism remains unclear. It has been found that phenotypic switching of vascular smooth muscle cells and pyroptosis are two biological processes closely related to the appearance and progress of AAA, which may become an important theory to reveal the mechanism of AAA and provide a new direction for the diagnosis and treatment of AAA. In this review, we will discuss the phenotypic switch of VSMCs and the regulatory relationship between cell pyroptosis and AAA.
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Recent progress of research into the role of lncRNA in the molecular mechanism of pulmonary hypertension

WU Daoxiong, LI Yanjin, HU Ying, WANG Yuming, HU Wei, MA Run

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Pulmonary hypertension (PH) is a fatal disease characterized by pulmonary vascular remodeling that ultimately leads to right heart failure and death. Current PH treatment is suboptimal, with no substantial improvement in the overall survival of patients with advanced PH. Despite the current partial progress has been made in the pathogenesis of PH, more exploration at the molecular level is needed to develop more effective treatments for PH. Recent researches have shown that long non-coding RNA (lncRNA) plays an important regulatory function in the pathophysiological process of PH, and has become a potential disease biomarker and therapeutic target. In this paper, we review the molecular mechanisms of lncRNA in PH in recent years.
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Research Progress of microRNA in the Field of Deep Vein Thrombosis

LILei, YUAN Qidong, PENG Xitao, ZHU Jin, PENG Juncai, HE Changhai, FU Liqing

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Micro-ribonucleic acid (miRNA) is a class of endogenous RNA molecules with a length typically ranging from 19 to 25 nucleotides.They regulate gene expression levels by identifying homologous sequences and intervening in transcription, translation,or epigenetic processes.miRNAs exhibit potential application value in the pathogenesis, progression,and treatment of deep vein thrombosis (DVT).DVT refers to the abnormal coagulation of blood within the lumen of the deep veins,blocking the venous lumen and leading to venous return obstruction, which is more common in the lower limbs.The detachment of thrombus into the lungs can lead to death.This article comprehensively reviews the diverse mechanisms of action of miRNAs in DVT in recent years.Given that the regulation of miRNA expression through targeted therapeutic approaches may promote the recovery of DVT,this article also discusses in detail the potential applications of miRNAs in the clinical diagnosis and treatment of DVT.This article aims to provide valuable references and insights for clinical and basic research in the field of DVT.
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Research progress of Wnt/β-catenin signaling pathway in programmed cell death after ischemic stroke

Panrui, Zhangming, Zhengxinyue, Wangchunxiao, Renqiongdi

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【】 Ischemic stroke (IS) is a neurological disease that damages brain tissue from insufficient blood supply to the brain due to blockage or stenosis of the brain vessels. In recent years, there has been increasing evidence that the Wnt/β-catenin signaling pathway plays an important role in the pathophysiological response to the occurrence and development of IS. Programmed cell death includes many forms such as apoptosis, necrotic apoptosis, pyrodeath, autophagy, panapoptosis and iron death. In this review, we will elucidate the characteristics of these different cell death modes and their cross-talk relationships with each other, and systematically outline the role of Wnt/β-catenin signaling pathways in the intervention of different cell death modes in IS, aiming to provide reference for future clinical and basic research.
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Comparison of stabilizing effect of different dose-bleomycin-induced pulmonary fibrosis in rats

songqinghua, tanghuimeng, sunxin, liuyang, xieyunyun, tianyange

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Objective: To compare the success rate and stability of rat pulmonary fibrosis (PF) models induced by intratracheal instillation of different doses of bleomycin (BLM). Methods: 150 SD rats were randomly divided into control group, low-dose BLM 3 mg/kg group (BL-L group), and high-dose BLM 5 mg/kg group (BL-H group). The general status, mortality, and weight changes of the rats were observed, the inspiratory capacity (IC), vital capacity (VC), chord compliance (Cchord) and dynamic compliance (Cdyn) of the lungs were detected on the 28th, 42nd, 56th and 84th days. Lung coefficients were recorded, pathological changes in lung tissue were observed by HE and MASSON staining, and collagen type III (COL III) expression in lung tissue was detected by immunohistochemistry. Results: (1) Mortality rate: The mortality rates of BL-L group and BL-H group were 20% and 28%. (2) Weight: The weight of the BL-L group was lower than that of the control group on days 0-56, and the weight loss was most significant on day 14 (P < 0.01), with weight recovery after day 56. From day 0 to day 56, the weight of the BL-H group was significantly lower than that of the control group and BL-L group (P < 0.01), and the weight gain remained relatively slow after day 56. (3) Lung function: compared with the control group, on day 28, the lung function of IC, VC, Cchord, and Cdyn were significantly lower in the BL-L group (P < 0.01, P < 0.05), and IC and Cdyn were significantly lower in the BL-H group (P < 0.01). On day 42, IC, VC, and Cchord decreased significantly in the BL-L group (P < 0.01, P < 0.05), while IC, VC, Cchord, and Cdyn significantly decreased in the BL-H group (P < 0.01, P < 0.05), and IC, VC, and Cchord were significantly lower compared with those in the BL-L group (P < 0.01). On day 56, Cchord was significantly lower in the BL-H group than in the control and BL-L groups (P < 0.01), and on day 84, there was no significant difference in lung function between the groups. (4) Lung coefficient: on day 28, the lung coefficients of the BL-L and BL-H groups were significantly higher than those of the control group (P < 0.01), and from day 42 to 56, the lung coefficients of the BL-H group were significantly higher than those of the BL-L group and the control group (P < 0.01), and on day 84, the lung coefficients of the groups did not differ significantly from those of the control group. (5) Lung histopathology and immunohistochemistry: inflammatory infiltration, fibrotic streaks and COL III expression were observed in the BL-L group from day 28 to 56, with the severity of the lesions decreasing over time, and the fibrotic lesions had almost disappeared on day 84, while in the BL-H group, significant fibrotic lesions could be observed from day 28 to 84, and the degree of COL III expression was significantly higher than that in the control group (P < 0.01). Conclusions: Both 3 mg/kg and 5 mg/kg BLM can successfully induce PF rat models. The PF model prepared with 3 mg/kg BLM developed fibrosis on day 28, which lasted until day 42 and gradually recovered. The PF model prepared with 5 mg/kg BLM showed fibrosis formation on day 28, and the degree of fibrosis was more severe than in the lower dose, with fibrotic lesions persisting stably up to day 56, and moderate-to-severe fibrosis still present in half of the cases until day 84.
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Research progress on the evaluation and intervention of social interaction behavior in animal models of autism

KONG Minghui, LU Liming, XIANG Leiying, CHEN Xiaoyi, ZHU Zhiru

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Autism Spectrum Disorder (ASD) is a highly heterogeneous neurodevelopmental disorder with a complex underlying genetic structure. However, preclinical trials currently under investigation for ASD mainly rely on rodent models to test the effects of non–pharmacological and pharmacological interventions on the core and related symptoms of ASD. This article elaborates on the brain regions that affect social interaction behaviors from the perspective of cognitive neural mechanisms; reviews behavioral testing experiments such as the three–chamber social interaction test, the visible burrow system, and the ecological HAB system; summarizes effective non–pharmacological interventions and pharmacological interventions such as baclofen, oxytocin, and metformin in the core and related symptom areas of ASD. This review aims to provide reference directions for promoting the development of preclinical trials using rodent models in the future.
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Study on the Pathology of Gouty Arthritis Based on Purinergic Receptor P2X7R

Wang Yinfeng, Liu Zeyu, Yin Xiaoyang, Lu Chengjin, Lin Zhijian, Zhang Bing

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Abstract: Objective: To observe the effects of Ice-Water Swimming on pathological changes in gouty rat model and investigate the regulatory mechanism of P2X7R therein. Methods: Male SD rats were divided into Normal group and Experimental groups, which included Gouty Control group, Ice-Water Swimming group and BBG group. Experimental groups were modeled to hyperuricemia and gouty arthritis by inhibiting uric acid metabolism combined with Coderre method. Ice-Water Swimming group were treated with 5 min of endurance swimming in an ice-water mixture at a depth of about 0.5 m for 0 h and 12 h after modeling by Coderre method, while the BBG group were injected intraperitoneally with BBG solution for 1 time immediately after modeling. Formula to calculate ankle swelling index. The serum uric acid level of rats was detected by uricase assay. The expression level of serum inflammatory factors IL-1β, IL-6 and TNF-α was detected by ELISA. HE staining was used to observe the pathological state of the subject ankle joints. Western Blot and Immunohistochemistry for P2X7R and NLRP3 Protein Expression in Synovial Tissue respectively. Results: Compared with Normal group, the serum uric acid level and ankle joint swelling index of Experimental groups were significantly higher (P < 0.05 or P < 0.01), and the synovial tissues all had different degrees of inflammatory infiltration. Compared with Gouty control group, the ankle swelling index of Ice-Water Swimming group was significantly higher at 12h (P < 0.05). The serum IL-1β, IL-6, TNF-α levels (P < 0.01) and the protein expression of P2X7R, NLRP3 in the synovial tissues were all significantly elevated (P < 0.05). Pathology results showed that the cartilage surface was broken. In addition, the synovial tissue showed severe hyperplasia and erosion, accompanied by a large number of inflammatory cell aggregates. There were no significant changes in P2X7R, NLRP3 protein expression and pathological damage in synovial tissues of BBG group compared with Gouty control group (P > 0.05), whereas the expression of serum IL-1β, IL-6, and TNF-α were all significantly suppressed (P < 0.01). Conclusion: Cold stimulation and strenuous exercise simulated by Ice-Water Swimming can exacerbate pathological damage in gouty arthritis by a mechanism that may be related to high localized P2X7R expression in the joints.
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Research progress on animal models of insomnia based on combination of disease and syndrome

ZHAO Zhongmin, LIANG Shuzhi, GAO Xiangye, HOU Suyu, LUO Dandan, WANG SHIjun, ZHANG Yan

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Insomnia, a prevalent clinical condition, not only diminishes patients" quality of life but also has the potential to give rise to further health complications. Traditional Chinese medicine has amassed and passed down knowledge about treating insomnia for thousands of years, resulting[1] in distinct advantages. It utilises syndrome differentiation and therapy to accomplish therapeutic effects by regulating the internal balance of the human body. To get a deeper understanding of how Traditional Chinese Medicine (TCM) treats insomnia, it is crucial to create animal models that exhibit symptoms closely resembling those found in humans with insomnia. This article provides a concise overview of the current disease-syndrome combination models, which may be classified into four categories: liver-depression, liver-depression for fire or liver-depression for spleen deficiency, heart-spleen deficiency, heart-kidney incompatibility, Yin and blood deficiency, This discussion will focus on particular modelling methodologies, assessment indicators, and model performance. The aim is to enhance the understanding of the pathophysiology of this disease in the context of traditional Chinese medicine. Additionally, this discussion aims to provide technical assistance for clinical efficacy evaluation and the creation of novel drugs.
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Current situation and countermeasures of laboratory animal license management in Hubei Province

liuconglin, qiaochuhua, liyanmei, chenxiaoli, zhangjinming, liudan, chenrui

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This paper introduces the daily management service of experimental animal license in Hubei Province and the supervision matters during and after the event. It expounds the current situation of experimental animal license management, achievements, problems and countermeasures in Hubei Province.The focus was on analyzing the legislative situation of experimental animals in Hubei Province, the issuance and distribution of permits, the scale of facilities, and the composition of employees. In recent years, the number of experimental animal licenses issued in Hubei Province has been increasing year by year, and the number of animal production and use by licensed units has continued to rise. While the related industries are flourishing, there are also some regulatory deficiencies. this paper from the perspective of biosafety, combined with the problems encountered in the license management service work, put forward the relevant safety supervision countermeasures and suggestions, so as to better promote the development of experimental animal industry in Hubei Province.
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Application research progress of single-cell sequencing technology in Multiple Sclerosis

MA Zhihong, ZHANG Lihong, CAO Yuan, CHENG Ming

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Multiple Sclerosis (MS) is a chronic autoimmune disease of the central nervous system (CNS) characterized by neuroinflammation and neurodegeneration. The pathogenesis of these diseases is complex, and a variety of central nervous system and peripheral cells are involved. In recent years, single-cell sequencing has gradually been applied in neurological disorder, which is of great significance for understanding intercellular heterogeneity, disease development mechanisms, and treatment strategies. This review will summarize the single-cell sequencing and its applications in MS.
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Mechanism study of mechanical stress mediated KOA synovial fibrosis through Piezo1/ERK1/2 axis

YuLikai, TianDi, SuZishan, JieLishi, GuoShaobo, WangPeimin, ZhangNongshan

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Objective To investigate the effect of Piezo1 activated by mechanical stress on KOA synovial fibrosis via ERK1/2 signaling pathway. Methods (1) Animal experiments: 25 SD rats were divided into blank group, exercise group, exercise +GsMTx4 group, exercise +PD98059 group, exercise +GsMTx4+PD98059 group, 5 in each group. After the modeling was completed, the serum and synovial tissue of rats were extracted and the collagen deposition was evaluated by Sirius scarlet staining and Masson staining. Western Blot and RT-qPCR were used to detect the expressions of Piezo1, ERK1/2, p-ERK1/2, α-SMA, TGF-β, Collagen I and TIMP-1, and the contents of IL-1β, IL-6 and TNF-α were detected by ELISA. (2) Cell experiment: the synovial cells were divided into five groups: blank group, pull group, pull +GsMTx4 group, pull +PD98059 group, pull +GsMTx4+PD98059 group. WB, RT-qPCR and other techniques were used to detect the above indexes in the molded cells. Results (1) Animal experiments: Mechanical stress increased Collagen deposition in synovial tissue of rats, and increased the protein and mRNA expressions of Piezo1, P-ERK /Erk, α-SMA, TGF-β, Collagen I and TIMP-1 of pathway-related and fibrosis-specific indicators (P< 0.05). The expression of Piezo1 was significantly down-regulated with both inhibitors (P< 0.05), but the ERK inhibitor (PD98059) had no significant effect on PIEZO1 expression. The content of serum inflammatory factors in exercise group was significantly higher than that in blank group (P < 0.05), and the improvement was obvious after the use of inhibitors (P< 0.05). (2) Cell experiment: WB and RT-qPCR results showed the same trend as animal experiments. Conclusion The Piezo1 ion channel can sense mechanical stress and activate the ERK1/2 pathway to mediate knee synovial fibrosis.
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Design and Application of Energy Monitoring System for Laboratory Animal Facilities

XU Xiao, XIONG Wenjing, MA Xixiang, MU Dandan, ZHOU Shunchang

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Objective The energy consumption of experimental animal facilities accounts for a significant proportion of the energy consumption in scientific research institutions, and its energy consumption characteristics are significantly different from those of ordinary buildings, thus requiring specialized monitoring and management. Method A set of energy consumption monitoring systems was designed for experimental animal facilities, and was deployed in the SPF-level experimental animal facility of Huazhong University of Science and Technology. Results After the system went online, it achieved real-time collection and recording of the facility"s electricity consumption data, and proposed energy-saving measures for three application scenarios. Conclusion The energy consumption monitoring system for experimental animal facilities has the characteristics of being reliable, efficient, and user-friendly, and has guiding significance and promotion value for the energy management work of experimental animal facilities.
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To study the effect of Houpu Sanwu decoction on exosomes of colorectal cancer model mice based on Rab27a

CHEN shu, RONG kang, ZHANG nan

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Objective: TO investigate THE effect and mechanism of Houpu Sanwu Decoction on subcutaneous tumor in C57BL/6J mice. Methods: Mouse colorectal cancer MC-38 cells were subcutaneously injected into C57BL/6J mice to establish a subcutaneous tumor model of colorectal cancer. The mice with successful model were randomly divided into model control group, Houpu Sanwu decoction low-dose group, Houpu Sanwu decoction medium-dose group, Houpu Sanwu decoction high-dose group, 5-fluorouracil group (5-FU group), and combination group (5-fluorouracil + Houpu Sanwu decoction medium-dose group), with 6 mice in each group. The mice were treated with normal saline and Houpu Sanwu decoction by gavage or normal saline and 5-FU by intraperitoneal injection once a day for 24 consecutive days. During the intervention period, the mental state, diet and other general conditions of mice were regularly detected, and the changes in tumor volume of mice were regularly detected. After sampling, the subcutaneous tumors of each group were weighed and the pathological changes of subcutaneous tumors were observed by HE staining Transmission electron microscopy, Western blot and NTA were used to identify the exosomes derived from colorectal cancer tissues. RT-qPCR and WB were used to detect the mRNA and protein expression levels of Rab27a and exosome markers CD63, TSG101, and ALIX in tumor tissues.Results: Houpu Sanwu decoction could inhibit the growth of tumor in mice. The tumor growth was slow in all dose groups of Houpu Sanwu decoction and its combination group, and the tumor growth was inhibited to varying degrees. The anticancer effect of middle dose of traditional Chinese medicine was the best, and the combination group showed synergistic effect with 5-FU. Houpu Sanwu decoction could induce tumor necrosis, showing the same anticancer effect as 5-FU group, and the higher the dose, the more serious the necrosis was. Moreover, Houpu Sanwu decoction combined with 5-FU showed synergistic effect. Houpusanwu decoction can inhibit the protein and mRNA expression of Rab27a and exosome specific markers CD63, ALIX and TSG101 in mice.Conclusion: Houpu Sanwu Decoction inhibits the secretion of exosomes regulated by Rab27a possibly by inhibiting the secretion of exosomes.
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Analysis of an animal model of hepatic encephalopathy based on the characteristics of clinical diseases in Chinese and Western medicine

liyaqing, wangcan, miaomingsan

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Objective To classify and analyze the existing animal models of hepatic encephalopathy based on the characteristics of Chinese and Western medicine clinical conditions, with a view to providing ideas for improving and perfecting the existing animal models of hepatic encephalopathy, so as to prepare animal models of hepatic encephalopathy that better meet the characteristics of the clinical conditions of Chinese and Western medicine combined with the conditions of hepatic encephalopathy. Methods In China Knowledge Network and Wanfang database, the Keywords "hepatic encephalopathy", "hepatic coma", "animal", "animal model" were used as Keywords, and in Pubmed database, "hepatic encephalopathy", "hepatic coma", " animal model", "animal" as the Keywords to search, collate effective literature with specific animal model preparation methods, collate and classify according to different modeling factors and methods, summarize the modeling methods and characteristics, and assess the clinical match of the animal model based on the characteristics of clinical diseases of hepatic encephalopathy in Chinese and western medicine. The clinical match of the animal model was assigned and analyzed according to the clinical symptoms of hepatic encephalopathy in Chinese and western medicine. Results There were 128 valid literature articles with 11 animal models, including 15 different modeling methods, among which, the CCl4 oil solution model had a high degree of agreement, and the highest degree of agreement in Western medicine was the CCl4 oil solution intraperitoneal injection+gavage+ammonium chloride intraperitoneal injection model (92%), and the highest degree of agreement in traditional Chinese medicine was the CCl4 oil solution intraperitoneal injection+ethanol aqueous solution self-drinking model (65%), but there was a lack of Chinese and Western medicine clinical disease characteristics.Conclusion The existing animal models of hepatic encephalopathy are all in accordance with the characteristics of the disease, but generally lack the manifestation of Chinese medicine, and lack of animal models combining the characteristics of Chinese and Western medicine. Combining the clinical characteristics of Chinese and Western medicine in the preparation of animal models is expected to provide a model basis for clinical diagnosis and treatment of hepatic encephalopathy, and point out the direction for the combination of Chinese and Western medicine in the treatment of hepatic encephalopathy.
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Establishment and optimization of a method for transferring golden hamster embryos using true pregnancy receptors

LAI Ya-na, ZENG Wen-tao

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Objective By optimizing the technical parameters of golden hamster embryo transfer, explore the optimal number and developmental period of transplanted embryos for golden hamster true pregnancy recipients. Methods By establishing a population of true pregnant albino golden hamsters as embryo transfer recipients, the effects of different embryonic development stages, recipient embryo reduction, and secondary transfer recipients on litter yield, donor embryo yield, and offspring survival rate were compared. Results Compared to wild-type golden hamsters as transplant recipients, true pregnancy albino receptors can quickly determine the origin of offspring and are suitable for various reproductive experimental programs based on embryo transfer. Fertilized eggs or two cell embryos have no significant impact on the transfer effect (P>0.05); The rate of donor embryos in the recipient embryo reduction group was significantly increased (22%, P<0.05), and the lower total number of births resulted in a significant decrease in cage survival rate (56%, P<0.01). The second transfer recipient"s non pregnancy rate was significantly increased (42%, P<0.01); The highest embryo yield rate (27%, P<0.01) and normal survival rate (89%) were observed in the transfer of 6-10 embryos. Conclusion The transfer of 6-10 donor embryos can help improve the yield and survival rate of donor embryos, We have successfully established an embryo transfer method using albino pregnant golden hamsters as recipients, providing technical support for the application and development of gene modification models in golden hamsters.
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Progress in the study of the regulation of rheumatoid arthritis-related pathways by external treatment of traditional Chinese medicine

ZHAO Ziying, WANG Guangyi

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Rheumatoid arthritis (RA) is an autoimmune disease with symmetric small joints pain as an early clinical manifestation, which gradually worsens and often involves multiple joints, ultimately resulting in arthritic deformities and loss of labor capacity. Molecular signaling pathways have always been the focus of research on the prevention and treatment of RA. Studies have found that the progression of RA disease is closely related to a variety of signaling pathways which include the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway, mitogen-activated protein kinases (MAPKs) signaling pathway, the NOD-like receptor protein 3 (NLRP3) signaling pathway, the toll-like receptors (TLRs) signaling pathway, the Wnt signaling pathway, Notch signaling pathway, hypoxia-inducible factor 1-alpha and vascular endothelial growth factor (HIF-1alpha/VEGF) signaling pathway, programmed death factor 1 and ligand 1 (PD-1/PD-L1) signaling pathway and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway. In recent years, the studies on the treatment of RA with external treatment of traditional Chinese medicine based on the above signaling pathways have gradually increased and deepened. In this paper, we reviewed the relevant data and reports to explain the relationship between the above pathways and the pathogenesis and prevention of RA and summarized the research results on the modulation of the above signaling pathways by external treatment of traditional Chinese medicine to prevent and treat rheumatoid joints with a view to providing a scientific basis for the clinical selection of this treatment.
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Study on optimization of preparation method of frozen section of skeletal muscle tissue

zhangjieyun, liangxinhua

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Objective To explore the optimal frozen section method for fresh and fixed skeletal muscle tissue, and to lay an experimental foundation for the rapid diagnosis of skeletal muscle diseases and the study of the pathogenesis of skeletal muscle diseases.Methods The tibialis anterior muscle of C57BL/6J mice was extracted, and the fresh tissue was treated by liquid nitrogen direct quick freezing, embedding agent combined with liquid nitrogen quick freezing, and foreign body alkane combined with liquid nitrogen quick freezing. The fixed tissues were pre-treated by direct embedding, embedding agent combined with liquid nitrogen quick freezing. After making frozen sections, HE staining was performed, and TISSUEFAX200 was used for scanning. The cross-sectional area of ice crystals and muscle fibers was calculated to evaluate the effect of different pre-treatment methods. Results The morphology of muscle fiber bundles disappeared and a large number of ice crystal vacuoles were observed in fresh tissues after liquid nitrogen direct freezing and foreign body alkane combined with liquid nitrogen freezing. The embedding agent combined with liquid nitrogen quick freezing ( the surface of the tissue is not in direct contact with liquid nitrogen ) shows that the muscle fiber bundle is complete and dense, and there is no ice crystal. It is a pre-treatment method suitable for fresh tissue. Fixed tissue directly embedded is not easy to slice ; after embedding agent combined with liquid nitrogen quick freezing treatment, the muscle fiber bundle was complete and there was no ice crystal.Conclusions The muscle fiber bundles of fresh and fixed tissues treated with embedding agent combined with liquid nitrogen quick freezing are complete and free of ice crystals, which is convenient for further experiments such as immunohistochemistry and immunofluorescence, and is conducive to the accurate and rapid diagnosis of skeletal muscle diseases and the exploration of the pathogenesis of skeletal muscle diseases.
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WEffect of Fuling Xingren Gancao granule on Polarization Phenotype Transformation of Atherosclerotic Macrophages

pengchaojie, wuhong

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Objective To explore the regulatory effect of Fuling Xingren Gancao granule (FXG) on macrophage polarization in atherosclerosis (AS) mice. Methods ApoE -/- mice were used to construct an AS model, while RAW264.7 macrophages were used to construct a polarized model. Oil red O and hematoxylin eosin staining (HE) were used to observe the total area of aortic plaques and the degree of aortic stenosis. PCR and Western blot were used to detect the expression levels, signal transduction, and transcription of M1 polarization factor inducible nitric oxide synthase (iNOS), monocyte chemotactic protein 1 (CCL2), M2 polarization factor arginase-1 (Arg-1), chitinase like protein 3 (YM1), and mannose receptor 1 (Mrcl or CD206) in vitro and in vivo. The phosphorylation level of signal transducer and activator of transcription (STAT3). Result: FXG significantly reduced the total area of aortic plaques in ApoE -/- mice, decreased the expression levels of M1 macrophage polarization factors iNOS and CCL2, and increased the expression levels of M2 macrophage polarization factors Arg-1 and YM1 (P<0.05). The phosphorylation levels of STAT3 in the model group mice and M1 macrophages decreased, but were upregulated after FXG intervention (P<0.05). The P-STAT3 inhibitor Stattic partially eliminated the regulatory effect of FXG on iNOS and Arg-1 (P<0.05).Result FXG significantly reduced the total area of aortic plaques in ApoE -/- mice, decreased the expression levels of M1 macrophage polarization factors iNOS and CCL2, and increased the expression levels of M2 macrophage polarization factors Arg-1 and YM1 (P<0.05). The phosphorylation levels of STAT3 in the model group mice and M1 macrophages decreased, but were upregulated after FXG intervention (P<0.05). The P-STAT3 inhibitor Stattic partially eliminated the regulatory effect of FXG on iNOS and Arg-1 (P<0.05).Conclusion FXG has an inhibitory effect on the progression of AS, which is related to the targeted regulation of macrophage polarization by STAT3.
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Research progress of nuclear factor E2-related factor 2 in oxidative stress after spinal cord injury

xihuilin, wujiajun, wangqingyan, baixinyue, hemengze, yangyanling

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Spinal cord injury (SCI) is a central nervous system disease with high morbidity, high disability and high mortality. A series of pathological and physiological changes after SCI, such as oxidative stress, will promote the further deterioration of the microenvironment at the site of injury, resulting in impaired neurological function. Nuclear factor E2-related factor (Nrf2) is a factor highly correlated with oxidative stress, so targeting the regulation of Nrf2 and alleviating oxidative stress may be one of the treatments for SCI. This article discusses the application of Nrf2 in post-SCI oxidative stress based on the occurrence of oxidative stress after SCI and the relationship between oxidative stress and Nrf2, and summarizes the strategies for targeting and regulating Nrf2, such as genes, non-coding RNAs and drugs, in the hope of providing new ideas for targeted therapy of SCI.
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Advances in the pathogenesis of abnormal copper metabolism disorder in Parkinson's disease

YANG Huijie, LAN Rui, WANG Manman, Wang Weiwei, LI Hongyu, TANG Chen, LIU Shuang, YANG Jieli, SHEN Xiaoming

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Parkinson's disease is a neurodegenerative disease associated with abnormal copper metabolism in the brain,which leads to misfolding and aggregation of α-synuclein-copper complexes, which is an important pathological sign of Parkinson's disease. Copper metabolism refers to the cellular metabolic process involving copper ions, which is closely related to the pathogenesis of α-synuclein aggregation, dopamine metabolism, mitochondrial dysfunction, oxidative stress and iron death in Parkinson's disease. In this review, we describe the molecular metabolic mechanism of copper toxicity by studying the pathological role of copper metabolism in Parkinson's disease，in order to provide evidence and help for further improvement of the mechanism of action and drug development.
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Study on the changes of intestinal permeability secondary to pig’s firearm penetrating wound of abdominal intestine in cold environment at high altitudes

QU Jinquan, LI Jiajia, LU Hongnan, YANG Xingyue, SUN Jiu, LIANG Feixing, WANG Yan, LIU Jiangwei

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Objective To observe the changes and possible mechanism of intestinal permeability in pigs without direct injury after abdominal intestinal firearm penetrating injury in plateau cold environment. Methods 55 experimental pigs were divided into two groups: plateau cold group (HC) and plain normal temperature group (LN). According to the observation time, each group was divided into five experimental subgroups: 0h, 2h, 4h, 8h and 24h. There were 6 pigs in each subgroup in HC group and 5 pigs in each subgroup in LN experimental group. According to the time point of euthanasia, intestinal tissues were taken and the levels of inflammatory factors TNF- α, IL6 and IL-10 in intestinal homogenate and the concentrations of intestinal permeability related proteins DAO and D-lactic acid in blood were detected by ELISA method. The intestinal tissues of experimental pigs were taken at LN-0h, LN-8h and HC-8h time points, and the intestinal pathological changes were observed and scored after HE staining. The contents of Occludin, ZO-1, Claudin-3 proteins related to intestinal permeability and TLR4, NF- κ B and MLCK proteins related to intestinal permeability were detected by WB method to explore the effect of cold environment at high altitude on secondary intestinal permeability changes after injury and its possible mechanism.
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Strain and gender differences in the behavioral models of chronic fatigue syndrome induced by Polyinosinic-polycytidylic acid and swimming in mice

TIAN Jiao, SU rui, WANG tingting, PEI Hailuan, WANG Jing

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Objective To compare the strain and gender differences between the ICR and C57BL/6J mice in the chronic fatigue syndrome model, and provide experimental evidence for the selection of model animals for chronic fatigue syndrome. Methods Mice were injected intraperitoneally with polyinosinic-polycytidylic acid (poly I:C) every three days and swam daily. The modeling was performed for 15 consecutive days, during which the weight and food intake of the mice were measured, and fatigue scores were assessed. After the modeling was completed, behavioral tests were carried out, including exhaustive swimming, tail suspension, mechanical pain threshold, and elevated plus maze. Results Compared with the control group, the exhaustion time of both strains of model mice in exhaustive swimming significantly decreased, the immobility time in tail suspension significantly increased, the mechanical pain threshold significantly decreased, the open arm entry time and frequency of the elevated plus maze in model male mice significantly decreased. The weight of model male C57BL/6J mice significantly decreased. The weight of model female ICR mice increased after the significant reduction. The exhaustion time of control C57BL/6J mice was significantly lower than that of control ICR mice. The immobility time of model C57BL/6J mice was significantly higher than that of model ICR mice. Conclusion There are differences between the two strains of mice in weight, fatigue level, and depression. Among the same strain of mice, there are differences between males and females, and the anxiety level of males is higher than that of females.
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The study of the mechanism by which EFHD2 regulates the NOX4/ROS pathway to initiate glycometabolism reprogramming and promote breast cancer progression

Xu ming fei, Zhang Yi, Kang ru yi, Liu chao yue

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Objective To investigate the mechanism of EFHD2 affecting the occurrence and progression of breast cancer based on NOX4/ROS signaling pathway. Methods The cells were divided into NC-shRNA group and EFHD2-shRNA group. The lentiviral vector silencing EFHD2 expression and its control vector were constructed and transfected MDA-MB-23 and MCF-7 breast cancer cells. The transfection efficiency was verified by qRT-PCR.CCK8 assay was used to detect cell proliferation activity. Plate cloning assay was used to detect cell colony formation ability. Scratch test was used to detect cell migration. Transwell assay was used to detect cell invasion. Flow cytometry was used to detect apoptosis and ROS levels. qRT-PCR was used to detect the mRNA expression of GLUT1, PDK1, PFK1, PKM2, PDH, and LDH. Western blot was used to detect the expression of Cleaved caspase-3, MMP-2 and NOX4 proteins. Results Compared with NC-shRNA group, EFHD2 expression was significantly decreased in EFHD2-SHRNA group, and cell survival and colony formation ability were weakened. The apoptosis rate and the expression of pro-apoptotic protein Cleaved caspase-3 increased. The cell migration distance was shortened, the number of cell invasion and the expression of MMP-2, which promotes migration and invasion, were decreased. The levels of lactic acid and GLUT1, PDK1, PFK1, PKM2 and LDH decreased, while the levels of ATP and PDH increased. Streaming results showed that ROS levels were reduced and NOX4 protein was down-regulated after silencing EFHD2. Conclusion EFHD2 can inhibit ROS production by regulating NOX4/ROS signaling pathway, cause lactic acid and glucose accumulation, promote apoptosis of breast cancer cells, and inhibit cell proliferation, migration and invasion.
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The Current Situation and Suggestions of Research on Laboratory Animal Welfare and Ethics in China

lihuiping, DENG Shaochang, YANG Jingchun, WEN Jingyin, ZHAO Weibo

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Objective? Exploring the current research status, research context, evolution process, and future research directions of laboratory animal welfare and ethics in China. Methods? Using literature related to laboratory animal welfare and ethics collected from source journals in the China National Knowledge Infrastructure (CNKI) database from 2001 to 2023 as the data source, a combination of qualitative description through literature review and CiteSpace visual bibliometric analysis was used to summarize the achievements, hot topics, and directions of laboratory animal welfare and ethics research. Results? Research shows that the overall popularity of research on the laboratory animal welfare and ethics in China is on the rise. The main research institutions include the systematic units of the Chinese Academy of Medical Sciences, the Nanjing General Hospital of the Nanjing Military Region, and the National Institutes for Food and Drug Control. The hot research topics in this field include the basic theories of laboratory animal welfare and ethics, legislation on laboratory animal welfare and ethics, technologies for laboratory animal welfare and ethics, censorship of laboratory animal welfare and ethics, and teaching research on laboratory animal welfare and ethics. In response to ethical issues arising from emerging interdisciplinary fields, continuous innovation is being made in research content. Conclusions? Suggestions have been put forward from the perspectives of legal system, censorship mechanism, education and training, and innovative research of laboratory animals welfare and ethics, with the purpose to provide reference and guidance for welfare and ethics work of laboratory animals.
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Evaluation of a nude mouse model of endometriosis fibrosis by the human xenograft subcutaneous transplantation method

zhouxue, wanguiping, zhangzhenzhen

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Objective To assess the feasibility of establishing a nude mouse model of endometriosis fibrosis of human origin and to determine whether endometrial mesenchymal stem cells are involved in inducing endometriosis fibrosis. Methods Four endometrial tissue specimens were collected and transplanted 1∶3 into 12 BABL/c nude mice by subcutaneous injection. The morphology and volume of the lesions were recorded, and the nude mice were executed on the 15th day after transplantation to observe the morphology of the lesions and their adhesion to the periphery of the abdominal wall, and HE staining was used to judge the results of modelling, Masson staining was used to assess the extent of fibrosis, and immunofluorescence was used to track the role of endometrial mesenchymal stem cells in the fibrotic process of endometriosis. Results The volume of ectopic lesions in nude mice increased over time, showing restricted, vesicular-like changes, with tight adhesion to the abdominal wall, endometrioid glands and collagen fiber deposition were seen microscopically, the success rate of modelling was 83.4%, and the collagen fiber volume fraction of the lesions was significantly higher after modelling (P<0.01), confocal imaging suggested that endometrial mesenchymal stem cells (SUSD2+) could differentiate into myofibroblasts (α-SMA+) in vivo. Conclusion The nude mice model established by the method of human allogeneic subcutaneous injection transplantation is consistent with the lesion characteristics of endometriosis fibrosis, which is simple and feasible, in addition to the in vivo observation that endometrial mesenchymal stem cells are involved in inducing the formation of endometriosis fibrosis, and it provides a better model reference for the further investigation of its pathogenesis.
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Research progress of the mechanism of medial prefrontal cortex layered structure in general anesthesia

lijia, yushouyang, luotianyuan, yutian

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The medial prefrontal cortex engages in various higher brain functions, including attention, transition of consciousness, and information integration, and becomes the central structure of action of general anesthetics. In addition, it is considered both the end point of the bottom-up model of layer-by-layer transmission of information and the starting point of the top-down modulation and integration of information. Classically, the medial prefrontal cortex can be divided into six layers in the vertical direction, with rich neural connections and different functions between layers. In this review, it describes laminar flow structures in the medial prefrontal cortex. Then, the review discusses that the general anesthetics change consciousness via cortical laminar flow structures. To this aim, the article reviews the available evidence in current studies from rodents, primates, and human studies that highlight the role of the medial prefrontal cortex in anesthesia.
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Transcriptome analysis of ethanol extract of Akebia trifoliate (Thunb.) Koidz on cell proliferation inhibitory functions and promote apoptosis in human liver cells

Wang Chunling, WenXiaodong

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Objective To investigate the effects and molecular mechanism of EEATK on proliferation, apoptosis of human hepatocellular carcinoma Hep3B cells and Huh-7 cells and to explore its underlying mechanism . Methods Human hepatoma cells Hep3B cells and Huh-7 cells cultured in vitro, blank control group, Sorafenib group (5uM), EEATK groups (0.10 mg/mL、0.15 mg/mL、0.20 mg/mL、0.3 mg/mL)were set and given corresponding drug intervention, respectively. CCK-8 assay was used to measure the viability of different interventions on the proliferation of Hep3B cells and Huh-7 cells, to screen the optimal action concentration for subsequent experiments. Hep3B cells and Huh-7 cells were divided into the blank control group and EEATK group(0.15mg/mL) treated with for 24 hours,EdU staining assay, colony formation assay were used to explore the effect of EEATK on the proliferation , the apoptosis rate,were detected by Annexin V-FITC/PI double staining assay.The transcriptome sequencing(RNA-seq)technology was used to analyze differentially expressed genes (DEGs) related to cell proliferation, apoptosis on Hep3B cells in blank control group and EEATK group(0.15mg/mL)of Hep3B cells, DEGs were analyzed for Gene Ontology(GO) function and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment. CTD (Comparative Toxicogenomics Database) was used to validate the expression of key proteins related to cell proliferation, apoptosis. Results Compared with the blank control group, different concentration of EEATK could significantly inhibit the activity of Hep3B and Huh-7 cells (P <0. 01) ; After treated with 0.15 mg/mL EEATK, the EdU positive cell rate and cell clone formation rate were significantly decreased (all P <0. 01), at the same time ,the apoptotic rates of EEATK group were significantly increased(P < 0.01). Compared with the blank control group, The transcriptome sequencing of Hep3B cells showed that EEATK induced significant changes in the expression of 1577 DEGs (P <0. 01) , of which 942 were up-regulated and 635 were down-regulated. GO functional enrichment analysis revealed that DEGs were mainly enriched in cholesterol synthesis, inflammation, and extracellular matrix. KEGG pathway analysis showed that EEATK may mainly pass through TFG- β Signal pathways and NF-κB signaling pathway plays an anti-tumor role.DEGs enrichment analysis showed that EEATK can significantly downregulate the expression of apoptosis related genes such as BIRC5 and CDK1 (P<0.01), the expression of CDKN1A and EGLN3 were significantly upregulated (P<0.01), At the same time, EEATK can cause significantly downregulation of cell proliferation related genes such as FAM83D and Ki-67 (P<0.01), mean while, the expression of MYC and FoxC1 were significantly upregulated (P<0. 01).
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Research progress on the improvement effect of Morinda officinalis oligosaccharides on depression

HE Mengjie, DAI Xueling, HUO Qing, LI Xin

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Depression is a psychosomatic disorder. In recent years, the rising incidence of depression around the world, bringing a heavy economic burden on society. The active substances extracted from the Chinese herb Morinda officinalis can soothe depression and calm the mind, tonify the kidney and benefit the intellect, and can also regulate monoamine neurotransmitter levels, enhance neuroplasticity, regulate the HPA axis, and regulate cytokine levels in antidepressant, as well as improve cognitive disorders in patients to a certain extent. Based on the hypothesis of the pathogenesis of depression, this paper summarises the role of Morinda officinalis oligosaccharides in antidepressant, and provides theoretical basis for the research and development of Morinda officinalis oligosaccharides antidepressant drugs.
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Research on potential dominant diseases of Traditional Chinese Medicine in the treatment of geriatric diseases based on bibliometrics

ZUO Yiming, SHI Guohua, LV Shichao, LIU Xuezheng

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Objective In order to effectively use the characteristics and benefits of traditional Chinese medicine in clinical therapy, bibliometric approaches are being used to investigate the Dominant diseases of traditional Chinese medicine in the treatment of Geriatric diseases. Methods The clinical research literature of traditional Chinese medicine in the treatment of Geriatric diseases in the past 10 years was retrieved from CNKI, Wanfang, VIP and CBM. The research trend and clinical efficiency of each disease were statistically analyzed to determine the potential dominant diseases of TCM treatment. Results A total of 22,859 articles were collected, with 3768 being included in the research. According to the International Statistical Classification of Diseases and Related Health Problems (ICD-11) of the World Health Organization, the diseases were classified into 17 categories and 149 diseases, primarily affecting the circulatory system, the skeletal musculoskeletal system or connective tissue system, and the digestive system. Conclusion Traditional Chinese medicine clinical trials on the treatment of geriatric illnesses cover a diverse spectrum of diseases, although the distribution is unequal. Potential dominant illnesses are eventually identified to include osteoporosis, constipation, and hypertension, with heart failure, stroke, coronary heart disease, diabetes and its complications, and insomnia being potential sub-dominant diseases.
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Exploring the effect and mechanism of action of secukinumab on calcific aortic valve disease based on IL-23/Th17 inflammatory pathway

lixinxin, zhangning, fengguangling, lanzhenzhen, guojiao, liuxincan

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Objective To observe whether the IL-23/Th17 inflammatory pathway is involved in the development of calcific aortic valve disease, and whether secukinumab can delay the progression of calcific aortic valve disease by inhibiting the IL-23/Th17 inflammatory pathway. Methods Forty-seven mice were divided into a blank control group, a model group, and a secukinumab group according to the random number table method. The blank control group was fed with normal chow, the model group and the secukinumab group were fed with pro-calcification chow for 16 weeks to establish a calcific aortic valve disease model, and the peak flow velocity changes of the aortic valves were detected under Doppler ultrasonography in all the mice after 4 weeks of intervention by secukinumab on the secukinumab group; relevant indexes were determined by HE staining, Von kossa staining, immunohistochemical staining, ELISA, and PCR. PCR were used to determine the relevant indexes. Results Compared with the model group, 4 weeks of drug intervention in the secukinumab group significantly reduced peak flow velocity ( P<0.05) and serum IL-6 levels ( P<0.05) in the aortic valve; compared with the secukinumab group, the leaflet thickness in the model group was significantly increased and there were more calcium deposits; Immunohistochemical results showed that macrophages ( P<0.05), IL-17A ( P<0.05), and IL-23 ( P>0.05) infiltration in the valve leaflets were reduced in the secukinumab group compared with the model group.PCR results suggested that the expression of STAT3, BMP-2 and α-SMA mRNA were significantly reduced in the secukinumab group compared with the model group ( P<0.05).Conclusion The IL-23/Th17 inflammatory pathway is involved in the pathogenesis of calcific aortic valve disease, and the inflammation, fibrosis, osteogenic differentiation, and calcification of mouse valves were alleviated after the intervention of secukinumab, which may delay the disease progression by inhibiting the IL-23/Th17 inflammatory pathway.
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Research development on the interaction between neuroimmunity and inflammation in the treatment of depressive disorder by traditional Chinese medicine

GUO Dong-jing, PAN Wen-chao, WANG Si-jia, MAO Qian-cheng, ZHAGN Hong-xiu, MA Ke

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As a common mood disorder, depression has a complex pathogenesis. In recent years, with the accelerated pace of people’s lives, the prevalence rate has increased year by year, attracting people extensive attention. External stress and inflammation jointly damage blood vessel and brain functions, induce immune disorders, cause microglia activation and increase the expression of pro-inflammatory cytokines and their receptors, inflammatory reaction continues to occur, which affects the normal metabolism and metabolism of the neurotransmitter system. Abnormal functioning of molecular pathways leads to mutations in brain cells and nerves, and the further formation of the immune-inflammation-neuron cycle path becomes an important mechanism in the occurrence and development of depression. a large number of studies have shown that Traditional Chinese medicine treatment can improve depression symptoms by restoring neuroimmune inflammation homeostasis. From the perspective of neuroimmune inflammation, this article explains its close connection with depression and its pathogenesis, and reviews the role of various traditional Chinese medicine antidepressant therapies in improving and treating depression by participating in the regulation of neuroimmune inflammation to provide a new angle of view for the precise treatment of depression and the development of immune-targeted drugs.
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Research progress on the mechanism of D-galactose-induced brain aging model: A review

ZHU Ziyue, JIN Meiling, XU Xiangyue, LIU Qing, ZHU Jiaxue, FU Mingjun, LEI Xia, ZHANG Ning

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As a normal physiological substance, D-galactose (D-gal) can induce a process similar to natural brain aging in vivo and in vitro under excessive intake, so it is widely used to induce brain aging model in China. The model of brain failure induced by D-galactose has the advantages of short time, low cost and significant effect, but its inducting mechanism is complex and diverse, and the relationships between the mechanisms are not clear, which leads to the limitation of the practical application of the model. This article reviews the in vivo metabolism of D-galactose and the various mechanisms of inducting brain aging, as well as the links between the mechanisms, in order to provide reference for the application and development of this model and the in-depth study of brain aging.
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Role of NLRP3-pyroptosis in experimental sepsis-induced lung injury

LI Yuting, NIU Chunyu, ZHAO Zigang

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Nod-like receptor pyrin domain-associated protein 3 (NLRP3) -mediated pyroptosis of pulmonary parenchymal and immune cells plays a key role in the pathogenesis of acute lung injury (ALI) during sepsis, and NF-?B, JAK2/STAT3, MAPK signaling pathways are involved in NLRP3-mediated pyroptosis. Targeting NLRP3-pyroptosis and its related signaling pathway, the pharmacological intervention of Physalin B, Schisandrin, 4-hydroxynonenal, Baicalin, GYY4137, and Erythropoietin, the physiatrics of acupuncture at Zusanli and Feishu, and the NLRP3 specific inhibitors such as Ergolide, play a good anti-septic effect on ALI. This article reviews the role and mechanism of NLRP3-pyroptosis in sepsis-induced ALI, as well as the experimental progress of targeting NLRP3-pyroptosis in the prevention and treatment of sepsis-induced ALI, hoping to take NLRP3-pyroptosis as the entry point to provide thinking for the formation of a new prevention and treatment strategy for sepsis-induced ALI.
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Effect of folic acid on the expression of Flotillin-1 and Aβ in the brain of mice with AD inflammation

Zewei MA, Li HUANG, Yunqin ZHENG, Meilin ZHANG, Huan LIU

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【Objective】To observe the effects of folic acid (FA) supplementation on the expression of Flotillin-1 and β-amyloid protein (Aβ) metabolism-related proteins in the brains of inflammation-stimulated AD mice.【Methods】Twenty-seven 6-month-old male APP/PS1 mice were randomly divided into AD, AD+LPS, and AD+LPS+FA groups, with 9 mice in each group. 9 same-month-old C57BL/6J male mice were used as the wild control group (Control). The AD+LPS+FA group was given folic acid supplemented feed (8 mg/kg) for three months of intervention, while the other three groups were fed normal feed. Lipopolysaccharide solution (LPS, 250 μg/kg/day) was injected intraperitoneally into mice in the AD+LPS group and AD+LPS+FA group one week before the end of the experiment, and saline was injected into the remaining two groups. The serum inflammatory factors TNF-α and IL-6 levels and brain tissue Aβ1-40 and Aβ1-42 levels of mice in each group were detected by ELISA, Flotillin-1 protein expression in brain tissue was detected by Western blot, and immunofluorescence double-labeling was used to detect the co-expression of Flotillin-1 in the cortical region of the brain and Aβ1-42/APP/PS1/ BACE1 co-expression. 【Results】 After ANOVA analysis, compared with the Control group, mice in the AD group had elevated serum TNF-α and IL-6 levels (P < 0.05), elevated levels of Aβ1-40 and Aβ1-42 (P < 0.05), increased expression of Flotillin-1 protein (P < 0.05), and increased co-expression of Flotillin-1 and Aβ1-42/APP/PS1/BACE1 in the cortical region of brain tissue (P < 0.05); Compared with the AD group, mice in the AD+LPS group had further increases in serum inflammatory factors and Aβ levels in the brain (P < 0.05), and increased expression of double-labeled positive proteins in the cortical region of brain tissue for Flotillin-1 and Aβ1-42/APP/BACE1 (P < 0.05) ; Compared with the AD+LPS group, mice in the AD+LPS+FA group had lower in vivo inflammation levels and Aβ content in the brain (P < 0.05), lower brain tissue Flotillin-1 protein expression (P < 0.05), and lower co-expression of Flotillin-1 with Aβ1-42/APP/PS1/BACE1 proteins in the cortical region of brain tissue (P < 0.05). 【Conclusion】 Folic acid supplementation may reduce Flotillin-1 protein expression and Aβ deposition in the brain of AD inflammatory mice.
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Practice and reflection on combining teaching and training to promote the standardization of animal experiments for medical postgraduates

CHEN Qin, LI Jianmin, GAO Yun, QIU Chen

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Standardized animal experiments are the basic prerequisite and important guarantee for eliminating potential biosafety risk factors and obtaining accurate medical research results. Professional training for graduate students who conduct animal experiments and strengthening publicity and education on animal experiment management regulations can help establish a sense of responsibility for standardizing animal experiments among medical graduate students. The innovative teaching-training model will fundamentally help to ensure the smooth implementation of animal experiments, and truly promote the healthy development of laboratory animal work in universities.
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The effect of Angelica sinensis polysaccharides on Th17/Treg cell balance and expression of related inflammatory factor proteins in bone marrow of mice with aplastic anemia

chenxiubao, xufei, yinxi, chenweida, cuixing, liuxiujuan, chenzetao

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Objective：To investigate the effect of Angelica sinensis polysaccharides on the balance of Th17/Treg cells and the expression of related inflammatory factor proteins in bone marrow of mice with aplastic anemia.Methods 50 male BALB/c mice were randomly divided into normal group,model group,cyclosporineA group,APS low and high dose groups.A mouse model of aplastic anemia was prepared by combining radiation irradiation with allogeneic lymphocyte infusion.After modeling,the mice were orally administered for 28 days.The general condition,weight changes,and spleen index of the mice were observed.Blood samples were taken to test the changes in basic hematological parameters of peripheral blood,and HE staining was used to evaluate the pathological changes in mouse bone marrow tissue;ELSIA method for detecting bone marrow TGF-β1.The expression levels of proteins such as IL-10,IL-17A,and IL-6;FCM detection of bone marrow Th17,Treg cell ratio,and Th17/Treg cell balance changes.Results Compared with the normal group,the model group mice showed clumsiness in activity,lethargy,pale eyelids,lips,and ears,and reduced food and water intake;Both body weight and spleen index significantly decreased;The peripheral blood red blood cell,white blood cell,platelet count,and hemoglobin concentration were significantly reduced;Disordered bone marrow tissue structure and significantly reduced proliferation of hematopoietic tissue;The expression of IL-17A and IL-6 proteins is significantly upregulated,and TGF-β1.The expression of IL-10 protein was significantly downregulated;The proportion of Th17 cells in bone marrow significantly increased,the proportion of Treg cells significantly decreased,and the ratio of Th17/Treg cells significantly increased(P<0.01).Compared with the model group,the general condition of the low and high dose APS groups improved,with an increase in food and water intake,a significant increase in body weight and spleen index,a significant increase in peripheral blood red blood cell,white blood cell,platelet count,and hemoglobin concentration(P<0.05),an improvement in bone marrow tissue structure,and an increase in hematopoietic tissue proliferation (P<0.05);The expression of IL-17A and IL-6 proteins is significantly downregulated,and TGF-β1. The expression of IL-10 protein was significantly upregulated(P<0.05 or P<0.01);The proportion of Th17 cells in bone marrow significantly decreased,the proportion of Treg cells significantly increased,and the ratio of Th17/Treg cells significantly decreased (P<0.01).Conclusion Angelica sinensis polysaccharides can improve bone marrow hematopoietic function in AA mice,and its mechanism may be achieved by regulating Th17/Treg cell balance.
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Analysis of ankylosing spondylitis’ animal model based on clinical characteristics of traditional Chinese and western medicine

Zhang Fangzhi, Miao Furui, Fan Yushan, He Yujun

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Ankylosing spondylitis is an autoimmune disease with sacroiliac arthritis and spinal arthritis as the main manifestations. The disease mainly occurs in young men, with a high disability rate and a serious threat to the life and health of patients. Biological agents are expensive, and there are many adverse reactions of hormones, non-steroidal anti-inflammatory drugs and anti-rheumatic drugs. Traditional Chinese medicine can regulate immunity and anti-inflammatory, and has a good clinical effect. In order to further study the pathogenesis of ankylosing spondylitis and the development and screening of therapeutic drugs, this paper summarizes the modeling method and mechanism of the existing animal model of ankylosing spondylitis, and analyse advantages and disadvantages of the model. To evaluate the coincidence of Clinical Characteristics of Chinese Medicine and Western Medicine,the paper compares the characteristics of Chinese and Western medical syndromes of the animal model. To build an animal model of ankylosing spondylitis with a higher degree of coincidence between traditional Chinese and western medicine is the key to innovative research of traditional Chinese medicine for treating ankylosing spondylitis. In order to lay a foundation for the research of traditional Chinese medicine for ankylosing spondylitis，this paper analyzes the degree of coincidence between Clinical Characteristics of Chinese Medicine and Western Medicine of animal model.
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Advances in bee venom research: novel drug candidate library for the treatment of inflammatory skin diseases

WU Qiang, Yang Yue, LI Peng, GU Jiajie, DONG Degang, YI Jun

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Inflammatory skin diseases (ISD) are characterized by persistent inflammatory infiltration and lingering and intractable skin lesions. At present, corticosteroids are the main drugs used in the treatment of ISD. However, due to the characteristics of recurrent and intractable ISD, long-term use of these hormone drugs may cause serious side effects to patients. In recent years, more and more studies have confirmed that bee venom (BV) has significant anti-inflammatory, anti-apoptosis, anti-fibrosis, antibacterial and other effects, so as to effectively treat ISD. In this paper, the main active components of BV are reviewed and its anti-inflammatory mechanism, and the latest status of BV in acne, atopic dermatitis, psoriasis, urticaria and systemic lupus erythematosus is discussed, which provides reference for the basic research and clinical treatment of ISD.
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Effect and Mechanism of Qishishenshu Capsule on Renal Fibrosis in Mouse Early Diabetic Nephropathy

LAO Xiao-qing, CHEN Chen, ZHANG Hong-min, YANG Xiu, SHI Jiang-shan, SU Hong-wei, SHEN Hong-ping, WANG Li, YOU Man-rui, LI Xiao-bin, ZHAO Chang-ying

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【Abstract】Objective To investigate the therapeutic effect and underlying mechanism of Qishishenshu capsule on renal fibrosis in mice with early diabetic nephropathy (DN). Methods DN mouse model was established by multiple injection of streptozotocin (STZ). The mice were randomly divided into the normal group (NC), model group (DN) and Qishi group (QS)(0.9 g/kg/d), 8 mice in each group, gavaged continuously for 4 weeks, and fasting blood glucose (FBG) was measured weekly. 4 weeks later, urinary microalbumin creatinine ratio (UACR), serum creatinine (SCr) and blood urea nitrogen (BUN) were measured. Hematoxylin-eosin staining (HE staining), periodic acid-Schiff staining (PAS staining) and Sirius red staining were used to analyze renal pathological changes. Real-time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was used to detect the Message RNA (mRNA) levels of fibronectin (FN), collagen type I alpha 1 (Col1a1), and α-smooth muscle actin (α-SMA). Immunohistochemistry (IHC) and Western blot (WB) were performed to detect FN, collagen type I (Collagen I), collagen type III (Collagen III), α-SMA, Podocin, Nephrin and transforming growth factor-β1/SMAD family member2/3 (TGF-β1/Smad2/3) pathway-related proteins. Results Compared with the NC group, mice in the DN group showed significantly higher levels of FBG and UACR (P<0.001). Mesangial hyperplasia, basement membrane thickening and collagen deposition occurred in renal tissue. The mRNA levels of FN, Col1a1 and α-SMA were increased (P<0.05). Protein levels of Podocin and Nephrin were decreased (P<0.05). The levels of FN, Collagen I, Collagen III, α-SMA and TGF-β1/Smad2/3 pathway protein were increased (P<0.05). Compared with the DN group, the level of UACR in QS group was decreased (P<0.05), and renal pathological injury was alleviated. The mRNA levels of FN, Collagen1 and α-SMA were attenuated (P<0.05). The protein levels of Podocin and Nephrin were elevated (P<0.05). Protein levels of FN, Collagen I, Collagen III, α-SMA and TGF-β1/Smad2/3 pathway protein were also decreased (P<0.05). Conclusions Qishishenshu Capsules improved renal fibrosis in DN mice probably through the inhibition of TGF-β1/Smad2/3 signaling pathway.
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Research progress of diarrhea animal model and its drug therapy

Shi Yucun, Dong Xiaoli, Hou Xiaoying, Yin Kai, Gao Fan, Wu Guotai

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Diarrhea is a common and frequently occurring disease in clinic, and there are many factors causing diarrhea. At present, there are many methods to study the animal model of diarrhea, but there are limited kinds of drugs to treat diarrhea in clinic, some of the drugs available also apply to single-factor diarrhea. Therefore, the establishment and selection of diarrhea animal model is not only an important basis for further study of the pathogenesis of diarrhea, but also an effective means for clinical screening and evaluation of all-round anti-diarrhea drugs. This article reviews the establishment and evaluation of animal models of diarrhea and the progress in the research of therapeutic drugs, in order to provide reference for the animal experimental research and drug prevention and treatment of diarrhea.
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Overexpression of TFB1M inhibits hepatocellular carcinoma cell migration and invasion

Tao Jia, He linli, wang li, ge pengsheng, sai shunhai

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Objective To explore the effect of transcription factor B1,mitochondrial,(TFB1M) on cell survival and migration of hepatocellular carcinoma cells and related molecular mechanisms. Methods TFB1M gene was overexpressed by transfection of eukaryotic recombinant plasmid. Cell survival and cell cycle distribution were detected by CCK-8 and flow cytometry. Cell migration and invasion were assessed by scratch healing and transwell chamber assays. Results The expression of TFB1M was significantly decreased in HCC, and the expression of TFB1M was more lower in female HCC patients than that tin male HCC patients. The mRNA expression of TFB1M was significantly increased after transfection of recombinant plasmid. Moreover, our results showed that overexpression of TFB1M had no effect on the growth and cell cycle distribution of HepG2 and Huh7 cells. However, overexpession of TFB1M remarkably attenuated the migration and invasion activity of HCC cells(all P<0.05). The results from the bioinformatics presented that the low expression of TFB1M might be related to the extracellular matrix assembly gene set in HCC. Conclusions TFB1M regulates the cell metastasis and invasion through influencing extracellular matrix assembly in HCC.
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Research progress on the mechanism of STAT3 in diabetic kidney disease

liuruidi, xujiangyan, xiezhishen, zhangxiaowei, chenjie, zhangzhenqiang

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Signal transducer and activator of transcription 3 (STAT3) is known to modulate expression related to cell transformation, proliferation and survival making it a significant target for cancer therapy. Recent research has also highlighted the crucial involvement of aberrant STAT3 activation in the pathogenesis of diabetic kidney disease (DKD). This paper aims to explore the therapeutic implications of targeting STAT3 in DKD, encompassing its structural characteristics, regulatory mechanisms of activity, pathological activation in DKD, and an overview of current research progress, with the objective of advancing understanding of DKD pathogenesis.
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Research Progress on Macrophage Metabolism and Immune Function in Coronary Heart Disease (CHD) with Phlegm and Blood Stasis Syndrome

CAO Panxia, PENG Zining, LI Jian, WU Hong

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In traditional Chinese medicine, coronary heart disease falls under the categories of "chest impediment and heart pain" and "true heart pain", with lipid metabolism disorder and inflammatory response acting as biochemical manifestations of "phlegm and stasis" throughout the disease. The energy metabolism of macrophages is closely related to their immune function and is an important factor in regulating the metabolic disorder and inflammatory response in coronary heart disease. This article reviews the role of macrophages in the pathophysiology of coronary heart disease, discusses how these metabolic pathways affect the immune response of macrophages, and how they influence the disease through energy metabolism pathways. It delves into the different modes of macrophage energy metabolism, especially the metabolic characteristics and immune regulatory functions of pro-inflammatory M1 and anti-inflammatory M2 macrophages in the syndrome of phlegm and blood stasis in coronary heart disease. This provides theoretical guidance for understanding the pathogenic mechanism of the syndrome of phlegm and blood stasis in coronary heart disease and developing new treatment strategies.
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Research progress on pharmacological mechanism of traditional Chinese medicine in the treatment of cerebral ischemia-reperfusion injury based on regulating AMPK signaling pathway

hechenfei, machiyuan, ranchunlong, chenghaoge, liuxiangzhe

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Cerebral ischemia-reperfusion injury(CIRI)refers to the recovery of blood supply after cerebral ischemia, leading to further damage and dysfunction of brain tissue. At present, modern medicine has made some progress in the prevention and treatment of CIRI, but it still faces some challenges and limitations. Therefore, it is of great clinical value to find effective interventions to prevent and treat CIRI. AMP-activated protein kinase(AMPK)and its downstream proteins are important targets for the treatment of CIRI and play a key role in the regulation of cellular energy homeostasis. Traditional Chinese medicine has the characteristics of multi-target, multi-pathway and multi-effect. It can activate the cascade reaction of AMPK signaling pathway, and treat CIRI by regulating autophagy, oxidative stress, inflammatory response and apoptosis, and has achieved certain results. Therefore, this paper summarizes the structure and mechanism of AMPK-related signaling pathway, elaborates its relationship with CIRI, and systematically summarizes the research status of traditional Chinese medicine regulating AMPK signaling pathway in the prevention and treatment of CIRI, in order to provide new ideas for the prevention and treatment of CIRI in traditional Chinese medicine and the development of new drugs.
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Effects of hypoxic preconditioning on NR2B in mouse hippocampal cell and HT22 cell

Wang Zhigang, Liu Xiaolei, yanlei, Wang Zhiguang, zhang Zhiyong, JIANG shuyuan, yang jing, Shao Guo

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objective: N-methyl-D-aspartate (NMDA) receptor subunit 2B (NR2B) and its phosphorylation are involved in cerebral ischemia/hypoxic neural injury. Hypoxic preconditioning (HPC) serves as an endogenous protective intervention to protect the brain from ischemic/hypoxic injury. This study intends to explore the effect of HPC on NR2B and its two tyrosine sites phosphorylation (1252 and 1336) in hippocampal cells through in vivo and in vitro experiments, and explore its role in HPC neuroprotection.
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Research progress on the mechanism of epigenetics in improving Parkinson"s disease through exercise

Liu Bo, Chen XiangHe, LuPengcheng, YangKang

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PD is a highly complex neurodegenerative disease, and its pathogenesis is influenced by DNA methylation, histone modification, and non-coding RNA. In research on Parkinson"s brain tissue and blood, it has been shown that changes in DNA methylation/histone modification levels, variations in ncRNA and its target genes may trigger or exacerbate the pathogenesis of neurodegeneration, and serve as potential non-invasive biomarkers for Parkinson"s disease. Exercise can improve neurodegenerative diseases caused by aging and PD by reversing epigenetics. This article reviews the pathogenesis of epigenetics in Parkinson"s disease, explores the role of exercise in it, and provides theoretical reference for improving Parkinson"s disease by regulating epigenetics through exercise.
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Inhibition of Boschniakia rossica Boschnaloside on Epithelial-Mesenchymal Transition of Hepatoma SMMC-7721 Cells

JIN Aihua, ZHU Jiebo, QUAN jishu

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Objective To investigate the inhibitory effect of Boschniakia rossica boschnaloside (BRBN) on epithelial-mesenchymal transition (EMT), invasion and migration of human hepatoma SMMC-7721 cells. Methods Transforming growth factor β1 (TGFβ1) was used to induce EMT model of SMMC-7721 cells. The cells were divided into the control group, model group and BRBN group. The cell migration was detected with wound healing test, the cell invasion was observed by transwell chamber assay, and the expressions of E-cadherin, N-cadherin, vimentin, Slug, Twist1, ZEB1 and signal transducers and activators of transcription 3 (STAT3) were determined with the western blot method. Results TGFβ1 resulted in the spindle-shaped changes in SMMC-7721 cells, down-regulated the expression of E-cadherin, and up-regulated the expression of N-cadherin and vimentin, suggesting that SMMC-7721 cells have obtained the mesenchymal phenotype. Compared with the model group, the expression of E-cadherin was significantly increased, expressions of N-cadherin and vimentin were reduced, expressions of Slug, Twist1, ZEB1 as well as STAT3 phosphorylation were also down-regulated in SMMC-7721 cells of BRBN group. Conclusions BRBN could inhibit the invasion and migration of human hepatoma SMMC-7721 cells, possibly by reversing EMT through STAT3 pathway.
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The Relationship Between Insulin Resistance, Hyperandrogenism, and Mitochondrial Oxidative Stress in PCOS

zhaoqi, yangliping, chenping, sunjianhua, mazibo

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Polycystic ovarian syndrome (PCOS) stands as a prevalent reproductive endocrine metabolic disorder within obstetrics and gynaecology. Two pivotal features of PCOS are insulin resistance (IR) and hyperandrogenemia (HA), both instrumental in its pathogenesis. There exists a discernible correlation between PCOS patients and mitochondrial oxidative stress, a relationship heavily influenced by various factors, notably insulin resistance and hyperandrogenemia. This article endeavors to elucidate the interplay between insulin resistance, hyperandrogenemia, and mitochondrial oxidative stress, while also exploring the impacts of insulin resistance and hyperandrogenemia on mitochondrial oxidative stress among PCOS patients.
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Research Progress on the Role of Microglia Efferocytosis in Alzheimer's Disease

Machiyuan, Wangxinzhi, Liuxiangzhe, Hanzhenzhen, Guoming, Lixiao

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Microglia efferocytosis is the process by which microglia phagocytose damaged and dead cells, with anti-inflammatory and pro-damage repair effects. Recent studies have shown that microglia efferocytosis plays a crucial role in the pathogenesis of Alzheimer"s disease (AD) and may be a novel therapeutic target for AD. This paper reviews the relationship between microglia efferocytosis and AD pathogenesis and the potential of efferocytosis-related molecules as therapeutic targets for AD. The aim is to provide new ideas and approaches for the treatment of AD.
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Research Progress on the Intervention of Tryptophan Metabolism in Alzheimer"s Disease

WU Cui, LI Canwei, ZHAO Hairong, YANG Zizhong, GAO Pengfei, ZHAO Yu, ZHANG Chenggui

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Alzheimer"s Disease (AD) is a degenerative neurological disorder that can lead to cognitive decline, mental behavior abnormalities, and reduced ability to daily lives. Tryptophan is an essential amino acid for the human body and is produced by three main metabolic pathways, namely kynuridine, 5-hydroxytryptamine (5-HT) and indole derivatives. Influencing the metabolites of tryptophan can lead to ameliorated neuroinflammation in the brain and significantly improvdcognitive ability, while the occurrence and development of AD.is affected and intervened. In this paper, we reviewed the research literature on tryptophan metabolism intervention in AD in recent 3 years from CNKI, PubMed and other databases.
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Role and mechanism of DNMT1 regulating LSM4 in HCY-induced hepatocyte apoptosis in mice

Xia Tongtong, Ma Fang, Liu Honglin, Zhang Zhenghao, Ding Hanshuang, Hao Yinju, Zhang Huiping, Wu Kai, Jiao Yun, Jiang Yideng, Li Guizhong

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Objective To study the effect of DNA methyltransferase 1 (DNMT1) on sm-like protein-4 (LSM4) in the hepatocytes apoptosis of mice induced by Hcy. Methods 12 ApoE-/- mice were divided into two groups: normal diet (ND, n = 6), high methionine diet (HMD, n = 6). Normal hepatocytes of NCTC1469 were divided into normal group (control, 0 μL/L Hcy), Hcy intervented group (Hcy, 100 μL/L Hcy), transfected NC siRNA control group (si-NC group, 0 μmol/L Hcy), transfected LSM4 siRNA group (si-LSM4 group, 0 μmol/L Hcy), transfected DNMT1 siRNA group (si-DNMT1 group, 0 μmol/L Hcy), transfected NC siRNA in the Hcy intervened group (Hcy＋si-NC group, 100 μmol/L Hcy), transfected LSM4 siRNA in the Hcy intervened group (Hcy＋si-LSM4 group, 100 μmol/L Hcy) and transfected siRNA DNMT1 in the Hcy intervened group (Hcy＋si-DNMT1 group, 100 μmol/L Hcy); Analysis of the expression of LSM4 in various tissues by NCBI database; quantitative real-time PCR (qRT-PCR) and Western blot (WB) were used to detect the difference of LSM4 protein expression in mice tissues (HMD and ND) and hepatocytes (control and Hcy). Western blot was used to detect the protein expression of Bcl2-associated X (Bax) and B-cell lymphoma-2 (Bcl-2). The cell apoptosis rate of control, Hcy, Hcy＋si-NC and Hcy＋si-LSM4 were detected by flow cytometry. MethPrimer online software was used to analyze the CpG islands of LSM4 promoter region. The expression of LSM4 in si-DNMT1 group was detected by qRT-PCR and Western blot. Results The expression of LSM4 in HMD/Hcy group was higher than that in the control group (P＜0.05). Bax protein expression in Hcy＋si-LSM4 was significantly higher than that in the control group (P＜0.05), but Bcl-2 was significantly lower (P＜0.05). The expression of Bax in Hcy＋si-LSM4 was significantly lower than that in Hcy＋si-NC group (P＜0.05), and the level of Bcl-2 was significantly increased. The cell apoptosis rate in Hcy group was higher than that in the control group (P＜0.05). The cell apoptosis rate in Hcy＋si-LSM4 group was lower than that in the Hcy＋si-NC group (P＜0.05). MethPrimer database analysis showed that the promoter region of LSM4 was GC rich and there was one CpG island. Compared with the Hcy+si-NC group, the expression of LSM4 protein in the Hcy+si-DNMT1 group was increased (P＜0.05). Conclusions DNMT1 regulates LSM4 hypomethylation to increase its expression, thereby promoting Hcy-induced apoptosis of mouse hepatocytes.
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Establishment of a multi factor induced hyperuricemic nephropathy rat model and study on the intervention effect of Qiling granules

Zhang Qian, Tu Hai Ye, Zhu Ke Yan, Yu Chen, Cai Yue Qin, Rong Yi Li, Zhang Li Zong, Chen Min Li, Fang Ming Sun

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Objective To establish a rat model of hyperuricemic nephropathy (HN) using a multifactorial induction method of potassium oxazinate combined with adenine and yeast feed, and to observe the intervention effect of Qiling granules (QLG). Methods Fifty-eight SPF grade male SD rats were selected, and ten rats were randomly selected as the normal control group. The remaining rats were induced by multiple factors to establish HN rat models. After 2 weeks of modeling, submandibular blood samples were taken to detect serum UA, CREA, BUN, TG, and TC. Forty HN rats with bleeding clearance UA and body weight close to the mean were selected. They were randomly divided into model control group, QLG low and high dose groups, and positive control group using a stratified randomization method, with ten rats in each group. Each group was given corresponding drugs by gavage daily, and after continuous administration for 4 weeks, submandibular blood samples were taken to detect serum UA, CREA, BUN, TG, and TC. After euthanasia of rats, and liver tissue was taken to detect XOD and ADA activity. Renal tissue was taken for HE and Gomori hexamine silver staining, and the protein expression of GLUT9, OAT1, VCAM-1, and TGF-β in the kidneys was observed using immunohistochemistry and WB methods. Results Compared with the normal control group, the serum levels of UA, CREA, BUN, TC, and TG, as well as liver XOD and ADA activities, were significantly increased in model control Group (P<0.01). The renal tissue of rats shows significant pathological changes. The positive area of urate in renal tubules and the expression of GLUT9, VCAM-1, and TGF-β proteins in the kidneys were significantly increased (P<0.01, P<0.05), while the expression of OAT1 was significantly reduced (P<0.01). Compared with model control group, the serum UA levels, liver XOD, ADA activity, and renal VCAM-1 protein expression of rats in each treatment group were significantly reduced (P<0.01, P<0.05). The serum CREA, BUN levels, and renal TGF-β protein expression of rats in the low-dose QLG group were also significantly reduced (P<0.05, P<0.01). The serum CREA, BUN levels, and renal GLUT9 protein expression of rats in the high-dose QLG group were also significantly reduced (P<0.01, P<0.05), and the urate deposition and renal injury caused by them in each treatment group were reduced to varying degrees, but there was no significant difference (P>0.05). Conclusion A stable HN rat model can be induced by gavage of potassium oxyzinate and adenine in combination with yeast feed to rats; QLG can effectively treat HN by improving UA metabolic disorders, reducing renal inflammation and urate deposition, as well as causing renal damage in HN model rats. Its mechanism of action is related to reducing serum UA, CREA, BUN, TG levels, liver XOD and ADA activities, as well as the expression of GLUT9, OAT1, VCAM-1, and TGF-β proteins in the kidneys.
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Ferroptosis and its role during experimental acute lung injury

guohuanrong, wang jing, zhao zi gang, niu chun yu

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Ferroptosis is a non-apoptotic mode of cell death characterized by iron-dependent lipid peroxides accumulation-induced membrane lipid peroxidation and mitochondrial atrophy, and differed from other programmed cell deaths in morphological and biochemical properties. Ferroptosis is regulated by a variety of metabolic pathways, involved in acute lung injury induced by hemorrhagic shock, ischemia-reperfusion, sepsis, and radiation. This article reviews the main regulatory mechanisms of ferroptosis and its role in the pathogenesis of acute lung injury in various animal models, with the aim of providing new strategies for the prevention and treatment of acute lung injury.
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Study of the mechanism of Honokiol protecting pulmonary microvascular endothelial barrier in LPS induced acute lung injury

Liu Jinxing

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Objective: To study the effect of Honokiol (HKL) on pulmonary microvascular endothelial cells in lipopolysaccharide (LPS) induced acute respiratory distress syndrome (ARDS) and its potential mechanism.Methods: Mouse lung microvascular endothelial cells (PMVEC) were cultured with DMEM+10%FBS in a six-well plate and divided into control group (Con group), Honokiol group (HKL group), Lipopolysaccharide treatment group (LPS group) and LPS+HKL treatment group (HKL+LPS group). The levels of Malondialdehyde and Reactive Oxygen Species in cell lysates were determined by TBARS assay kit and H2DCF-DA, respectively. TUNEL/DAPI double staining was used to detect apoptosis. The cell junction was detected by VE-cadherin/DAPI and Claudin-5/DAPI double staining. Western blotting was used to detect caspase-3, cleaved caspase-3, Sirt3, SOD2, and acetylated SOD2 (Ac-SOD2). 32 mice were randomly divided into control group (Con group), Honokiol group (HKL group), Lipopolysaccharide treatment group (LPS group) and LPS+HKL treatment group (HKL+LPS group). HE staining was used to observe the pathological changes of lung tissue.Results: Honokiol pretreatment could significantly reduce LPS-induced increase of ROS and MDA levels, and decrease LPS-induced increase of SOD2 acetylation and SIRT3 down-regulation. TUNEL and Caspase analysis showed that Honokiol could protect apoptosis of PMECs induced by LPS. VE-cadherin fluorescence staining demonstrate thag Honokiol pretreatment could prevent LPS from damaging cell adhesion. Claudin-5 fluorescence staining show that Honokiol pretreatment could prevent LPS from disrupting tight connections of cells. In animal experiments, HE staining showed that Honokiol significantly inhibited the typical pathological changes of ARDS in the lung tissue of mice in LPS group.Conclusion: HKL can significantly inhibit LPS-induced oxidative stress, apoptosis and cell connection breakdown of pulmonary microvascular endothelial cells, thereby alleviating ARDS symptoms.
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Preliminary studies on the mode of CdCl2 in combination with nicotine on spermatogonial cells

han xue, jiang li, zhang yuan, wu de sheng, huang hai yan, liu jian jun

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Objective：To investigate the combined effect of CdCl2 and nicotine on the cell cycle and apoptosis of mouse spermatogonium(GC-1).Methods：CCK-8 assay was used to detect the inhibition of GC-1 cell proliferation in the CdCl2 groups, the nicotine groups, and the combined groups at 24 hours. Flow cytometry was used to detect the effects of the CdCl2 groups, the nicotine groups, and the combined groups at 24 hours on the cell cycle and apoptosis of GC-1 cells. Results：The inhibitory effect on the proliferation of GC-1 cells was increased with the rise of CdCl2 and nicotine concentrations , the IC50 values of CdCl2 and nicotine alone was 5.409μmol/L, 2814μmol/L. When CdCl2 and nicotine were used in combination, the IC50 value of GC-1 cells was 4.422 μmol/L for 0.175 mmol/L nicotine, 4.532 μmol/L for 0.35 mmol/L nicotine, 3.309 μmol/L for 0.7 mmol/L nicotine, and 2.532 μmol/L for 1.4 mmol/L nicotine ,all of which were lower than that of the groups in which CdCl2 was used alone. The combination of CdCl2 and nicotine had a synergistic effect. At a CdCl2 concentration of 2.5 μmol/L, the IC50 concentration of the combination group was lower than that of nicotine alone. The results showed that percentage of G0/G1 phase cells was decreased in the 2.5 μmol/L CdCl2 group and 1.4 mmol/L nicotine group; compared with the CdCl2 groups and the nicotine groups, percentage of G0/G1 phase cells was decreased in the CdCl2 and nicotine combination groups; percentage of G2/M phase cells was increased in the 2.5 μmol/L CdCl2 group, and compared with the CdCl2 groups and nicotine groups, the cells were blocked in G2/M phase in the combined groups. Combined effects of CdCl2 and nicotine on the cell cycle had a synergistic effect , and the effect of CdCl2 on the synergistic effect was stronger. Proportion of cell apoptosis was increased in 2.5μmol/L CdCl2 group. Compared with the CdCl2 groups and the nicotine groups, percentage of cell apoptosis in the CdCl2 and nicotine combined groups were increased significantly, and the effect of CdCl2 was stronger for the synergistic effect. Conclusion：Combination of CdCl2 and nicotine had a synergistic effect on mouse spermatogonium(GC-1) which could lead to enhanced cytotoxicity, G2/M cell cycle arrests, and cell apoptosis. And CdCl2 was the main effect factor of synergistic effect.
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Molecular mechanism of autophagy mediated by AKT/mTOR pathway involved in exercise rehabilitation of rotator cuff tear-related muscle atrophy

tangjing

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objective: To explore the molecular mechanism of autophagy mediated by protein kinase B(AKT)/ mammalian target protein of rapamycin (mTOR) pathway in the rehabilitation of muscle atrophy associated with rotator cuff tears (RCTs). Methods: Forty male C57 mice were randomly assigned to the following four groups: sham group, RCTs group, RCTs+ exercise group and RCTs+ exercise+rapamycin group, with 10 mice in each group. At the eighth week after grouping, the healing of bone-tendon interface and muscle cell atrophy were analyzed by histology. The mRNA expression levels of muscle atrophy related genes (Atrogin-1, Bnip 3, MuRF-1) in supraspinatus muscle tissue were measured by real-time quantitative reverse transcription polymerase chain reaction. The expression of LC3 and AKT/mTOR signal pathway in supraspinatus muscle tissue of different groups was detected by western blot, and the production of autophagy in each group was analyzed by transmission electron microscope. Results: Compared with sham operation group, the maturity score of bone-tendon interface at supraspinatus tendon anchorage and the cross-sectional area of supraspinatus muscle fibers in RCTs group decreased significantly (P<0.001), and the muscle loss and the expression of Atrogin-1, Bnip 3 and MuRF-1 genes increased significantly (P<0.001). Compared with RCTs group, RCTs+ exercise group significantly increased the bone-tendon interface maturity score and the cross-sectional area of supraspinatus muscle fibers (P<0.01), and decreased the muscle loss and the expression of Atrogin-1, Bnip 3 and MuRF-1 genes (P<0.01). Compared with the sham group, the LC3Ⅰ/LC3Ⅱ and number of autophagy in supraspinatus muscle of RCTs group increased significantly (P<0.001), while the p-Akt/Akt, p-mTOR/mTOR decreased significantly (P<0.01). Compared with RCTs group, the LC3Ⅰ/LC3Ⅱ and number of autophagy in RCTs+ exercise group decreased significantly (P<0.01), and the number of p-Akt/Akt and p-mTOR/mTOR increased significantly (P<0.001). The addition of rapamycin significantly inhibited the improvement of exercise on bone-tendon interface healing, muscle atrophy and loss, AKT/mTOR signaling pathway and autophagy number induced by RCTs. Conclusion: This study confirme the anti-atrophy effect of exercise rehabilitation in RCTs diseases, and its mechanism is related to activating AKT/mTOR signal to inhibit autophagy.
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The overview of traditional Chinese medicine in regulating the mechanism of regulatory cell death in vascular dementia

lihui, Dongxingang, Liweifeng

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Vascular dementia (VD) is a neurodegenerative disease caused by brain injury, the research on the process of its occurrence is not yet in-depth. The regulatory all death (RCD) mechanism is related to the pathological mechanisms of VD, including apoptosis, pyroptosis, autophagy, ferroptosis, and copper mediated cell death proposed in recent years. Therefore, explain the role between the mechanisms of regulatory death and the pathological mechanisms of VD, is of beneficial for the study of VD. The article provides a review of the roles of five mechanisms of RCD in VD, and summarizes the recent research progress in the treatment of VD with traditional Chinese medicine, in order to development of new traditional Chinese medicine drugs.
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Research progress on animal models of malignant mesothelioma

YONG Sheng, JIN Dacheng, dong xin chun, GOU Yunjiu

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Malignant mesothelioma cases are rare and have a long incubation period, making it difficult to conduct clinical research.? Animal models of malignant mesothelioma are crucial for experimental research and elucidating the pathogenesis for malignant mesothelioma. Common animal models include spontaneous, inducible, transplantable, and genetically engineered models, but the applicability of different animal models varies. This article reviews studies related to the establishment of animal models of malignant mesothelioma in the past 10 years and summarizes the recent progress in the establishment of four animal models of malignant mesothelioma from three aspects: modeling methods, modeling results, and model advantages and disadvantages. This review summarizes and analyzes the current progress in the establishment of inducing animal models of malignant mesothelioma, this provides a reference for malignant mesothelioma basic research using animal models.
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The effect of ovariectomy on cognitive function and hippocampal estrogen receptor expression in APP/PS1 mice

congchao, Gu zuxi, Wu panqing, Chen siru, Lin guangyao, Xu lianwei

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Abstract: Objective: The present study aims to observe the changes in Aβ deposition and estrogen receptor levels in the hippocampal tissue of female APP/PS1 mice with Alzheimer's disease (AD) after ovariectomy (ovx) at different ages. Method: 3-month-old APP/PS1 female mice were divided into 3 groups, with 20 mice in each group. 10 mice in each group were treated with bilateral ovarian resection via abdominal surgery as the model group. 10 mice in the control group (sham group) were treated with only equivalent volume fat removed from the corresponding area during surgery as the control group (sham group). Feed APP/PS1 mice at different ages for 3 months, 4 months, and 5 months as the 6-month, 7-month, and 8-month age groups. Evaluate the cognitive function of APP/PS1 mice at different ages using Morris water maze. Observe the morphological changes of intracellular organelles in the CA1 area of the hippocampus of the two groups of mice using transmission electron microscopy. Immunofluorescence staining is used to detect the deposition of Aβ in the CA1 area of the hippocampus of the two groups of mice. ELISA is used to detect the levels and contents of serum estrogen, ROS, SOD, and MDA, and Western blot is used to determine the expression levels of ERα and ERβ. Result: As the age increased, the escape latency of the ovx group mice in the water maze test gradually prolonged, the deposition of Aβ in the hippocampal CA1 area increased, the mitochondrial swelling of hippocampal neurons increased, and a large amount of lipofuscin and amyloid deposition were observed in the cytoplasm. The serum estradiol level and SOD activity decrease, while the ROS level and MDA content increase. The expression of ERα and ERβ in hippocampal tissue decreases. Conclusion: Ovariectomy in mice with low estrogen status may exacerbate hippocampal Aβ deposition and age-dependent cognitive decline.
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The Effect of Western Dietary Feed on the Model of Atherosclerosis in APOE Mice

wanglei

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Objective To study the rapid modeling of Western dietary feed and its impact on biological indicators and histopathology in APOE-/- mice.Methods Using 48 female、48 male APOE-/- mice, 48 female、48 male C57BL/6J mice was tested and divided into 8 groups, namely the APOE-/- ordinary breeding feed group (24 female and 24 male each）、 APOE-/- Western Dietary Feed Group (24 female and 24 male each）、 C57BL/6J ordinary breeding feed group (24 female and 24 male each）、C57BL/6J Western Dietary Feed Group. Feed from 3w until the end of the experiment at 20w. After the experiment, serum was collected for biochemical indicators, and the aorta was separated for gross oil red staining and analysis. The root of the aorta was paraffin sectioned and HE stained. Results Western diet did not significantly increase APOE- / -body weight, western diet could significantly improve the blood lipid index of APOE- / -mice, total cholesterol, low density lipoprotein, high density lipoprotein, promote the formation of atherosclerotic plaque, male mice are suitable for the modeling of gross aortic plaque, and female mice are suitable for plaque modeling of aortic arch root. Conclusion Western dietary diet can promote APOE- / -mice, increase the aortic plaque area ratio, shorten modeling time, and improve modeling uniformity.
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Screening of antidiarrhea active parts and study on the “spectrum-effect” relationship of salt-processed Alpiniae oxyphyllae Fructus -Foeniculi Fructus medicines

li hongwei

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Objective To screen the antidiarrheal active components of salt-processed Alpiniae oxyphyllae Fructus -Foeniculi Fructus medicines (YZYH), and speculate on its pharmacological substance basis and quality markers through the study of the “spectrum-effect” relationship. Methods A model of diarrhea due to spleen and kidney yang deficiency was established in rats, and the pharmacodynamic indexes of YZYH on petroleum ether, ethyl acetate, and water fractions were measured, including behavioral indicators such as body weight, anal temperature, diarrhea incubation period, diarrhea index, and biochemical indicators such as NOS, cGMP, and CPK; Establish HPLC chromatograms of different parts of YZYH, and use grey correlation method to analyze the “spectrum-effect” relationship between the chemical components of each part of YZYH and the antidiarrheal efficacy indicators. Results In the aspect of pharmacodynamics, the ethyl acetate fraction had a better regulatory effect on the activities of DIP, DI, and serum NOS, cGMP, CPK in model rats compared to other treatment groups; In terms of the study of the “spectrum-effect” relationship, the correlation between components such as anisaldehyde and chromatographic peak 4 with the five efficacy indicators of DIP, DI, NOS, cGMP, and CPK was strong. Conclusion The ethyl acetate fraction was the active anti diarrhea fraction of salt-processed Alpiniae oxyphyllae Fructus -Foeniculi Fructus medicines. Its mechanism may be realized by regulating gastrointestinal peptide hormones such as MTL and GAS, inhibiting gastrointestinal hyperfunction, regulating energy metabolism and immunity, and cytoprotection; The ingredients such as anisaldehyde and peak 4 served as the material basis for its antidiarrheal effect, and anisaldehyde and peak 4 could be used as quality indicators for the medicines.
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Exploring the analgesic initiation mechanism of tuina on the dorsal root ganglion of minor CCI model rats via the TRPV1/TRPA1 -cGMP signaling pathway

YANG Zhenjie, YU Tianyuan

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Objective: To explore the analgesic initiation mechanism of the three-manipulation and three-acupoint of tuina on rats with minor CCI model. Methods: 56 SD rats were randomly divided into 8 groups: normal group, sham group, model 1 group, model 2 group, tuina 1 group, tuina 2 group, tuina 1 + TRPA1 antagonist group, and tuina 2 + TRPV1 antagonist group. The model group, tuina group, and tuina + antagonist group were established with minor CCI models. The tuina group and tuina + antagonist group received the three-method three-point intervention (point method, dial method, kneading method, Yinmen point, Chengshan point, Yanglingquan point) 7 days after modeling. The model group and sham group were subjected to grasping restraint, and the normal group was not intervened. After the intervention, each group was tested for changes in thermal withdrawal latency (TWL) and mechanical withdrawal threshold (MWT) to detect different types of pain. The nitrate reductase method was used to observe the NO content in the DRG of each group on the modeling side, and ELISA, Western blot, qPCR, and other methods were used to observe the changes in the protein and gene expression of the TRPV1/TRPA1-NO-cGMP-PKG signaling pathway in the DRG of each group on the modeling side. Results: Compared with the model group, behavioral testing showed that the MWT and TWL were prolonged to varying degrees in the tuina 1 group and tuina 2 group. The expression of TRPV1, TRPA1, NO, sGCβ, cGMP, and PKG1 in the DRG of the tuina 1 group, tuina 2 group, tuina 1 + TRPA1 antagonist group, and tuina 2 + TRPV1 antagonist group were significantly decreased. Conclusion: Tuina intervention can effectively improve the symptoms of thermal and mechanical hyperalgesia caused by peripheral nerve injury after one intervention. Tuina can exert immediate analgesic effects through the TRPV1/ TRPA1-NO-cGMP-PKG signaling pathway.
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Establishment of intestinal polyps animal model with Apc-KRAS-Cre genetic mutation

TAN WEI SHAN, WANG SHU YUN, WANG HAO YUE, SUN KE XIANG, GAO JIA MIN, DENG WAN LI

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Abstract: Objective To create the mice model of colorectal polyps with Apc-KRAS-Cre gene mutation with the best tamoxifen induction method. Methods C57CL/6J mice were used as healthy control group. Genetically mutated mice were grouped and intraperitoneally injected with tamoxifen of different concentration and dosage for different durations. The survival rate and change in weight of mice were observed. 4 weeks post-tamoxifen induction, mice were euthanized and the length of colons, amount and size of intestinal polyps were observed. Through H&E staining, the histopathological changes of the intestinal tissue and polyps were observed. Results The survival rate of male mice is higher than that of female mice(P<0.05), while the survival rate between the 4 groups shows statistical significance(P<0.05). When compared to the healthy control group, the changed in weight and the length of the colons of each group of mice showed statistical significance（P<0.001）, (P<0.05), the difference in weight change between group 1 and group 2, group 2 and group 3, group 1 and group 4; the difference in length of colons between group 1 and group 3 showed statistical significance (P<0.05). Each group of mice induced by tamoxifen injection showed intestinal polyps of varying sizes, mostly occuring on the distal end of the colon, while those in group 3 and group 4 have a higher amount and larger polyps. Comparing to healthy control group, histopathology of tamoxifen-induced mice showed growth of intestinal polyps, with uneven and misaligned glandular and epithelial arrangements, loosely-packed intestinal mucosal barrier and irregularly-distributed crypts, group 3 and group 4 mice showed signs of inflammation, while regions of group 4 showed necrosis of cells. Conclusion Tamoxifen-induced Apc-KRAS-Cre mice models have been successfully established, with group 3 induction method being the most suitable.
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The method and improvement of implantable osmotic pump for intraventricular drug administration in rats

SUN Heyong, ZHANG Gangli, WU Jiliang, CAO Peili, LI Shuo, SUN Haoqin

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Objective To introduce and enhance the experimental technique for intraventricular drug delivery via an implantable osmotic pump. Methods Eight-week-old male SD rats were selected, and the requisite equipment and reagents were prepared. Initially, the osmotic pump was assembled and brought to operational status before conducting the implantation surgery. Following anesthesia, the animals underwent skin preparation, and the skull's upper surface was surgically exposed. Utilizing a brain stereotaxic apparatus, a point directly above the ventricle was located, and a small hole was drilled at that location with a high-speed cranial drill. Subsequently, the pump body was implanted subcutaneously in the neck, the needle was inserted into the drilled hole, and secured with dental cement. Once solidified, the needle base was removed, the subcutaneous soft tissue and scalp were sutured in layers, and the animal was returned to its cage for isolated rearing. Results The osmotic pump was successfully implanted subcutaneously in the rat's neck, the needle was securely affixed to the skull, and the catheter interface remained intact. Upon examination of the extracted brain tissue, no significant hematoma was observed around the puncture site or needle tract, and the presence of blue dye in the ventricular and adjacent tissues indicated successful drug delivery to the ventricle. Conclusion The introduction of a brain stereotaxic apparatus for localization assistance, coupled with enhancements to the operational procedure, has rendered the implantation process more accurate and safe, achieving a high success rate in intraventricular drug administration.
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The positive effect of the good operation of the CNAS-CL06 system on the scientific nature of animal experimental

maliying, wanghong, guomeng, liangchunnan, yuebingfei, gongwei

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The animal laboratory of pharmaceutical and biological product inspection and testing institutions undertakes important basic support tasks for testing and scientific research work. This article summarizes the management experience accumulated in the operation of our institution's CNAS-CL06 quality management system, providing reference for similar institutions in operation to ensure the scientific nature of animal experimental data. In order to ensure the scientific nature of animal experimental data, the experimental animal institution has successfully passed the CNAS accreditation of the experimental animal institution, and has completed rectification on time during on-site supervision and evaluation. At the same time, regular self inspections of the system have been carried out in accordance with the "Quality and Capability Accreditation Guidelines for Experimental Animal Breeding and Use Institutions" (CNAS-CL06). During the self inspection process, we examined issues while improving the content of the system. Starting from animal procurement, occupational health and safety, animal disease treatment and care, and facility operation emergency drills, we enriched the content of the quality management system, ensured the continuous and effective operation of the system, and ensured the effectiveness and standardization of animal experiment data. At the same time, we contributed to the management ideas of our institution in sharing animal experiment platforms, Provide hardware and software support for the construction of cloud platforms for animal experiments. This article aims to explore and form a quality management model for the experimental animal industry based on practical work, Being focused in the standardization strategy， continue to deepen the reform of standardization work, and give full play to the basic and strategic role of standardization in the modernization of the animal experiments system.
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Management and experience exchange of three-level laboratory of animal biosafety in University

tianxiaoyan, Yangwenhao

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Animal Biosafety Level 3 laboratory (Absl-3) is the basic supporting platform of the national biosafety system for new and recurrent infectious diseases, it provides an important hardware basis for the study of biological characteristics, prevention and treatment of highly pathogenic microorganisms. ABSL -3 laboratory also provides an important support for the combination of production, teaching and research. The normal operation of ABSL -3 laboratory and the smooth development of scientific research work can not be separated from the careful planning and effective implementation of emergency planning work. In addition, the reasonable design and layout of the laboratory is also a key factor to avoid and reduce accidents. Based on the practice of construction and management of animal biosafety level III Laboratory in Yangzhou University, starting with the preparation of emergency plan, this paper introduces the points for attention in the layout of laboratory construction, daily operation and emergency treatment, it is expected to provide useful reference for biosafety laboratories operating various pathogenic microorganisms in the future.
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Research progress on the mechanism of miR-138-5p in osteoarthritis

Wu Liangbin, Weng Jian, Li Aikang, Qi Tiantian, Zhang Geng, Zeng Hui, Yu Fei

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MiR-138-5p, as a microRNA, plays an important regulatory role in the pathogenesis of osteoarthritis. It regulates various biological processes such as inflammation, cell apoptosis and proliferation, and matrix degradation in osteoarthritis by modulating signaling pathways including NF-κB, Wnt/β-catenin, and PI3K/AKT. This review summarizes the research progress on the mechanism of miR-138-5p on osteoarthritis.
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Preliminary Discussion on the Existing Issues of Ethical Review of Laboratory Animals Welfare in Medical Research

wang xiao xiao

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Laboratory animals have played an important role in maintaining human health. Advocating ethics and welfare of laboratory animals is a dual manifestation of technological progress and human civilization, and establishing ethical review of laboratory animals welfare is an effective guarantee for achieving the welfare of laboratory animals. Although the construction of animal welfare ethics in China has developed rapidly in recent years, there are still many problems that need to be continuously improved at this stage. This article is based on the understanding and recognition of the ethical concepts related to the welfare of laboratory animals. It summarizes and discusses some issues discovered during the ethical review of laboratory animals welfare in medical research, and puts forward personal suggestions for exchange and mutual refrence.
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Research progress of the role of ferroptosis in infectious diseases

YUE Linzhi, MA Tao, DAI Yumei, DU Wenya, WANG Guofu, WU Lixian

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Ferroptosis is a newly discovered mode of programmed cell death characterized by the accumulation of intracellular iron-dependent lipid peroxidation. At present, the research on ferroptosis mainly focuses on the field of cancer, but more and more evidence shows that ferroptosis is related to the occurrence of infectious diseases, and ferroptosis has been found in Corona Virus Disease 2019, tuberculosis and cryptococcal meningitis and other diseases. This article reviews the role of ferroptosis in infectious diseases, in order to provide new ideas for the prevention and treatment of ferroptosis related infectious diseases.
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Oxidative stress-based exploration of the zebrafish in cardiovascular disease and research progress

Fei Tiantian, Liang Tengyun, Wu Hong

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Cardiovascular disease has been a serious threat to human life, and oxidative stress is an important factor in the occurrence and development of cardiovascular disease. The construction of reliable animal models of oxidative stress is helpful for in-depth study of the pathogenesis of cardiovascular diseases and the development of therapeutic drugs. Zebrafish, with the advantages of easy reproduction, short developmental cycle, transparent embryos for easy observation, and highly homologous cardiovascular gene background with humans, has often been used in recent years for research related to the field of cardiovascular diseases. In this paper, we focus on the application of zebrafish oxidative stress model in cardiovascular disease and the related research progress, which provides reference for its further application in cardiovascular disease related research.
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Effects of ezrin protein on Helicobacter pylori-induced nodular gastritis

Wang Peng, Zhu Hong-wei, Jiang Shuy-uan, Liu Xiao-lei, Gao Bin, Shao Guo

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The ERM protein family (ezrin, radixin, and moesin) plays a pivotal role in cell morphology, migration, and signal transduction. Ezrin, a prominent member of this family, is highly involved in these processes. Particularly, the phosphorylation of ezrin is crucial, as it regulates the interaction between ezrin and the actin cytoskeleton. This interaction is a key mediator of cytotoxicity in host cells infected with Helicobacter pylori, significantly impacting cell morphology. This review comprehensively summarizes the multifaceted role of ezrin protein in Helicobacter pylori-induced nodular gastritis. It delves into the relationship between ezrin"s structure, function, phosphorylation, and signaling pathways in the context of nodular gastritis. Moreover, this paper highlights ezrin protein as a potential therapeutic target, offering novel insights for the prevention and treatment of nodular gastritis.
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Research progress on mitochondrial-associated membranes (MAMs) in the pathogenesis of Alzheimer's disease

liushiyu, xuyumin, xuhongcai, lufangmei

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Mitochondrial-associated membranes (MAMs) is a special domain for communication and material exchange between mitochondrial outer membrane and endoplasmic reticulum membrane, which performs various biological processes of cell life activities under different conditions. MAMs dysfunction-mediated calcium homeostasis imbalance, endoplasmic reticulum stress, mitophagy defects, mitochondrial fission/fusion dynamics imbalance, lipid metabolism disorders, and inflammatory responses are the key pathogenesis of Alzheimer’s disease (AD). This article reviews the structure and function of MAMs, their involvement in AD pathology and drug intervention targets, and discusses the role of MAMs in the pathogenesis of AD and the latest mechanism research progress, in order to provide new ideas for the prevention and treatment of AD.
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Research progress on Mitochondrial Damage in Inflammatory Bowel Disease

WU Xiaoting, XUAN Ang, SHEN Juan

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Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory disorder of the gastrointestinal tract that poses a significant threat to human health. The pathogenesis of IBD remains unclear and is believed to involve various factors such as genetics, immune dysregulation, and environmental triggers. In recent years, increasing evidence has highlighted the role of mitochondrial damage and dysfunction in the development of IBD. This review provides a comprehensive review and overview of studies related to mitochondrial damage in inflammatory bowel disease, focusing on the effects of mitochondrial oxidative stress damage, autophagy dysfunction, kinetic disturbances, and respiratory defects on IBD. The aim is to identify potential therapeutic targets and provide new insights for the scientific prevention and treatment of IBD.
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miR-22-3P targets GSDMD to inhibit homocysteine induced pyroptosis of vascular smooth muscle cells

ZHONG Yingyi, Ding Ning, Wang Yicheng, Liu Chao, Ma Shengchao, Xiong Jiantuan, Hao Yinju, Bai Zhigang, Jiang Yideng

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Objective To investigate the effect of miR-22-3p on pyroptosis of vascular smooth muscle cells induced by homocysteine. Method Human vascular smooth muscle cells (VSMC) were cultured in vitro and divided into the Control group (0 μmol/L Hcy) and the Hcy group (100 μmol/L Hcy). After intervention, Western Blot was performed to detect the expression of Pro Caspase-1, GSDMD, N-GSDMD and NLRP3. The qRT-PCR was used to measure the expression of miR-22-3p. ELISA was utilized to survey the concentration of IL-1β and IL-18 in the supernatant. After transfection with control of miR-22-3p (miR-22-3p-NC) ，mimic of miR-22-3p (miR-22-3p-mimic) , and inhibition of miR-22-3p (miR-22-3p-inhibitor) ， to observe the change of VSMC pyroptosis induced by homocysteine. Result Compared with Control group, the expression levels of Pro Caspase-1, GSDMD, N-GSDMD, NLRP3 in VSMC of Hcy Group were increased (P<0.05) , the concentration of Il-1β,IL-18 were higher (P<0.01) , and the relative expression level of miR-22-3p was lower (P<0.01) . After transfection with miR-22-3p-mimic, the expression levels of Pro Caspase-1, GSDMD, N-GSDMD and NLRP3 in VSMC decreased significantly (P<0.01) , and the concentrations of il-1β and IL-18 decreased significantly (P<0.01) . After transfection with miR-22-3p-inhibitor, the expression levels of Pro Caspase-1, GSDMD, N-GSDMD and NLRP3 in VSMC increased significantly (P<0.01) , and the concentrations of il-1β and IL-18 were higher (P<0.05) . Conclusion miR-22-3p delayed Hcy induced VSMC pyroptosis.
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Dioscin promotes apoptosis of HepG2 cell through inhibiting Wnt/β-catenin signaling pathway

liangyuqiong, huangqing

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Objective ?To detect the effects of apoptosis on HepG2 cell induce by Dioscin and its possible mechanism of anti-hepatocellular carcinoma. Methods The HepG2 human hepatocellular carcinoma cells were exposed with 0.25,0.5,1,2,4,6,8 μmol/L dioscin, and then the cell proliferation ability was measured with
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Evaluation of pulmonary arteriolar lesions in rats induced by cigarette smoke exposure combined with Klebsiella infection

REN Zhouxin, ZHAO Peng, LI Jiansheng

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Objective To analyze the morphological and structural changes of pulmonary arterioles in rats induced by smoke exposure combined with Klebsiella infection, and to evaluate the severity of pulmonary arteriolar lesions. Methods Pulmonary arteriolar images of lung sections of control rats and model rats induced by smoke exposure combined with Klebsiella infection were analyzed by qualitative and quantitative methods. Victorian blue stained sections were used for the detection of pulmonary arteriolar muscularization, vascular wall thickness, vascular occlusion score, intima thickness and media thickness of muscular arterioles, and neointima proliferation. HE stained sections were used for the observation and detection of inflammatory cell infiltration and plexiform lesions around arterioles. VG stained sections were used for the observation of collagen fibers in the intima and detection of the percentage of collagen fibers area in arteriolar wall area. Based on the above results, the degree of pulmonary arteriolar lesions was rated according to the Heath-Edwards criteria. Results For diameter ≤ 50 μm arterioles, compared with the control group, the percentage of non-muscular vessels was significantly decreased, the percentage of muscular vessels was increased, the percentage of partial muscular vessels was not significantly different, the wall thickness of non-muscular vessels and the wall thickness of muscular vessels were significantly increased, and the occlusion scores of both non-muscular and muscular pulmonary arterioles were significantly increased in the model group. For 50 < diameter ≤ 100 μm arterioles, compared with the control group, the percentage of non-muscular vessels was significantly decreased, the percentage of muscular vessels and the percentage of partial muscular vessels were not significantly different, the wall thickness and occlusion score of muscular vessels were significantly increased, the wall thickness and occlusion score of non-muscular vessels were not significantly different in the model group. Compared with the control group, the intimal thickness and media thickness were significantly increased and the perivascular inflammatory infiltration score was significantly increased in muscular arterioles with both diameter of ≤ 50 μm and 50 < diameter ≤ 100 μm of the model group. In the control group (n=9), only one section with neointimal lesion was found with 1.61 % of proliferation degree of neointima. In the model group (n=10), five sections had neointima lesion from 1.04 % to 17.14 % of proliferation degree of neointima, respectively. No plexiform lesions were found in a11 sections. For pulmonary arterioles with diameter of ≤ 100 μm, there was no change in the expression of intimal collagen fibers in the model group compared with the control group, and there was no significant difference in the percentage of collagen fiber area in the vessel wall area. According to the Heath-Edwards criteria, the pulmonary arteriole lesions in the model rats did not reach grade III. Conclusions The model rats show pathological manifestations such as pulmonary arteriolar muscularization, thicking intima and media, and mild to moderate inflammatory reactions around arterioles. The low degree of neointimal proliferation and collagen fiber in the vascular wall and no plexiform lesions suggest that the model is up to grade II lesion according to the Heath-Edwards criteria.
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Progress of animal experimental research on the treatment of Henoch-Schonlein Purpura with TCM

Su Hang, Zhang Shuzi, REN Xianqing

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Henoch-Schonlein purpura (HSP) is the most common systemic vasculitis in childhood, which is called "spot toxin", "purpura wind" and "grape plague" in TCM. Modern medical research suggests that the disease is related to factors such as imbalance of cellular and humoral immunity, abnormal secretion of cytokines, disturbance of coagulation and fibrinolysis mechanism, but the exact pathogenesis is still unclear. The incidence of this disease increasing year by year, with a high recurrence rate and a high proportion of kidney damage, which seriously affects the physical and mental health of the[[基金项目] 国家自然科学基金（82374519,U2004107）；河南省青年科学基金项目（232300421309）；河南省中医药科学研究专项（20-21ZY2161） [作者简介] 苏杭（1988-），男，副主任医师，硕士研究生，研究方向：中医药防治小儿肾病及风湿免疫性疾病 Email：362504467@qq.com [通信作者] 任献青（1973-），男，教授，主任医师，博士研究生，研究方向：中医药防治小儿肾病及风湿免疫性疾病 Email：renxq723@163.com ] affected children and poses a great social risk. Numerous studies have shown the clinical efficacy of TCM in treating HSP, but its mechanism of action is not yet completely clear. In recent years, a large number of animal experiments have been carried out to study the efficacy mechanism of TCM with the establishment of animal models of HSP, but there is a lack of a more systematic and detailed reviews. Therefore, the animal experimental literature related to the treatment of HSP with TCM in the past decade were reviewed, and the effects of TCM in alleviating abnormal glycosylation of IgA1, regulating the immune imbalance of Th1/Th2 and Treg/Th17 cell, reducing circulating immune complex, and inhibiting inflammatory responses were compiled and summarized, In order to providing a reference for the further research on TCM for the treatment of HSP and inspiring new research ideas.
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Progress of miRNA in the pathogenesis of pulmonary hypertension

LI Yanjin, XIAO Liying, WU Daoxiong, GUAN Rong, YAN Chunlang, LEI Wen

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Pulmonary hypertension(PH) is a progressive disease characterized by pulmonary vascular remodeling. Current treatments for PH remain suboptimal, and there is an urgent need to better decipher the underlying pathomechanisms in order to find new therapeutic targets. miRNA(microRNA) are key components in the post-transcriptional machinery that mediate cellular functions mainly by regulating the expression of downstream target genes. Numerous in vivo and in vitro studies have demonstrated the involvement of miRNA and their regulators in PH development. However, there is no unified conclusion about the mechanism of miRNA regulation of pulmonary vascular remodeling. Therefore, this article provides a review on the mechanisms of miRNA in PH in recent years.
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[ ]Establishment of sterile golden hamster model

GUO ya-xi, duxiaopeng, liukaihui, wangzhaohua, zhuhua

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Abstract：【Objective】 A sterile golden hamster model was established by cesarean section purification method.【Methods】The donor female golden hamsterrats selected SPF grade golden hamster, male and female were mated 1:1, and were separated from male rats after meeting the peg. The cage time of the surrogate mothers rats should be one week earlier than that of the donor mothers. The pregnant parturient golden hamsters underwent hysterectomy in a super-clean workbench. at the time of delivery, andThe uterus were transferred into isolation kits for purification. The uterus wasand stripped to obtain the milk mice to be purifiedfor purification, . and sterile Sterile ICR mice and sterile SD rats were respectively used for milk replacement, and transferred to isolation kits for feeding after successful milk separation. The sterility status of feeding isolation kits is tested monthly. 【Results】Three caesarean sections were performed, but the first and second lactation failed. The third milk replacement was successful, and 18 young rats hamsters were obtained with survival rate of 88% and survival rate of 66% after milk release. All of them hamsters were qualified according totested by GB /T 14926.41-2001.【Conclusion】By cesarean section purification technique, sterile ICR mice and sterile SD rats were used for milk replacement to achieve the purpose of microbial purification, and the sterile golden hamster model was obtained.
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Inhibitory effect of 17-DMAG on PD-1 humanized mouse liver cancer transplantation tumor

LI Xiaojuan#, XIU Ye#, LI Xingjie, SUN Yanfeng, LI Ruisheng

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Objective Explore the inhibitory effect of 17-DMAG on the growth and angiogenesis of PD-1 humanized mouse liver cancer transplantation tumor. Methods 30 PD-1 humanized mice were selected and human HepG2 cell suspension was injected into the subcutaneous tissue of the right inguinal region of the mice to construct a human liver cancer transplant tumor model. Tumor bearing humanized mice were randomly divided into three groups (10 mice per group): ① model group (injected with 10 mg/kg of physiological saline); ② 17-DMAG group (intraperitoneal injection of 17-DMAG at 25 mg/kg, 3 times/week); ③ The cisplatin group (intraperitoneal injection of 20 mg/kg, 2 times per week), the experiment lasted for 4 week. After injection, the length and short diameter of the humanized mouse transplanted tumor were measured to calculate the volume, and the tumor mass were measured to calculate to calculate the tumor inhibition rate. At the same time, immunohistochemical methods were used to detect the expression of CD31 (tumor microvessel density, MVD) and vascular endothelial growth factor (VEGF) in tumor tissue. Results The tumor volume and mass of the 17-DMAG group and the cisplatin group were significantly reduced compared to the model group (P<0.05), and the tumor inhibition rate of the 17-DMAG group was slightly higher than that of the cisplatin group. However, there was no significant difference in tumor mass, volume, and tumor inhibition rate between the 17-DMAG group and the cisplatin group. The number of MVD labeled microvessels and VEGF expression in the 17-DMAG group and cisplatin group were lower than those in the model group (P<0.05), and the 17-DMAG group was also lower than those in the cisplatin group (P<0.05). Conclusions 17-DMAG can inhibit the growth of humanized mouse liver cancer xenografts by reducing the expression of vascular endothelial growth factor in liver cancer xenograft tissue, thereby inhibiting the generation of tumor neovascularization.
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Research progress of liver fibrosis based on Notch signal pathway

jishaoxiu, zhanghengyao, zhangyuan, wenli

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Liver fibrosis is a necessary pathological process from chronic liver disease to cirrhosis and even liver cancer. The occurrence of liver fibrosis is a highly integrated and dynamic pathological process resulting from the interaction of many cells and cytokines. Notch signaling pathway is an evolutionarily conserved intercellular signal transduction mechanism, which plays an important role in regulating the development and tissue renewal of multicellular animals. More and more studies have shown that Notch signal transduction participates in the formation of liver fibrosis through a variety of ways. Therefore, this paper reviews the role of Notch signaling on cells involved in the formation of liver fibrosis to explain the function of Notch signaling pathway in liver fibrosis.
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Construction and evaluation of an immunosuppression-mediated model of invasive Aspergillus niger lung disease in rats

TANG Zining, CHEN Xiangchi, LIU Xuewu, ZHOU Zhimin, LI Qiao, XIAO Sa, JIANG Dejian, PENG Dongdong

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Abstract: Objective This study establishes a model of invasive Aspergillus niger lung disease in immunosuppressed rats to provide theoretical support for the pharmacodynamic evaluation of anti-invasive pulmonary aspergillosis drugs and mechanism studies. Methods Sixty SD rats were randomly divided into a normal control group, a cyclophosphamide control group, and a cyclophosphamide + fungal infection low, medium, and high dose group, with 12 animals in each group. General clinical observations were performed daily, and the serum levels of immunoglobulin G (IgG), immunoglobulin M (IgM) and serum galactomannan (GM) were detected by ELISA on the 3rd and 7th days of modeling, respectively, as well as the ratio of CD4+ and CD8+ cells and the content of white blood cells (WBCs) and neutrophils (Neu) in peripheral blood, and the load of Aspergillus niger in alveolar lavage were observed simultaneously and morphological changes of rat lung tissue. Results The rats in the cyclophosphamide control group and the cyclophosphamide+fungal infection group showed reduced voluntary activity and erect hair after modeling, and the rats in the cyclophosphamide+fungal infection group were accompanied by shortness of breath and audible wet rhonchi in the lungs; compared with the normal control group, the rats in the cyclophosphamide control group showed significant reductions in the levels of CD4+, WBC, Neu, IgG and IgM in the blood, and the proportion of CD8+ was significantly higher (P<0.05, P<0.01); compared with the cyclophosphamide control group, rats in the cyclophosphamide+fungal infection group showed significant decreases in blood levels of CD4+, WBC, Neu, IgG, IgM, and significant increases in levels of CD8+, GM, and the alveolar lavage load of Aspergillus niger (P<0.05, P<0.01); and the lung tissues of the cyclophosphamide+fungal infection rats in the low-, medium-, and high-dose groups showed mycelial distribution and destruction of alveolar epithelium, increase of bronchial epithelial cup cells in the alveoli, and infiltration of inflammatory cells, and the degree of lesions was positively correlated with the modeling dose. Conclusion In this study, we used Aspergillus niger combined with cyclophosphamide immunosuppressant to construct a model of invasive Aspergillus niger lung disease, and the duration of the disease was positively correlated with the concentration of the bacterial fluid and the modeling time, which confirms that the cellular immunity plays an important role in the pathogenesis of the disease, and at the same time the immunoglobulin can also affect the development of the disease process of invasive pulmonary aspergillosis, and it is speculated that the pathogenesis of invasive pulmonary aspergillosis may be related to the level of immunoglobulin in the humoral immunity.
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Educational reform of animal experiment course for medical graduate students: cultivating students" ability of active learning and innovative thinking

MIAO Jinxin, MIAO Mingsan

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Animal experiment course is an important practice teaching link in medical and life science. It is of great significance to the cultivation of students' experimental skills, scientific thinking and innovative ability. However, the traditional teaching method of animal experiment course has the problems of single content and low participation of students. In order to promote students' active learning and innovative thinking, this paper aims to discuss the teaching reform of animal experiment course. Firstly, the paper introduces the background and significance of the teaching reform of animal experiment course and emphasizes its importance to the cultivation of students' ability. Secondly, it puts forward the principles of teaching reform of animal experiment course, including student-centered, paying attention to problem solving and practice exploration, and promoting interdisciplinary integration. Then, from the aspects of course design, teaching methods and evaluation methods, this paper expounds the concrete measures of teaching reform of animal experiment course in detail. In the course design, attention should be paid to the selection of challenging and exploratory experimental projects, and students' interests and professional needs should be fully considered. On teaching methods, students should be encouraged to actively participate in, exploration and cooperation, and guide them to problem solving and the cultivation of innovative thinking. In terms of evaluation methods, diversified evaluation methods, such as experimental report, group discussion and project presentation, should be used to comprehensively evaluate students' comprehensive ability and innovative thinking. Finally, through practical verification and effect evaluation, the experience and results of the teaching reform of animal experiment course were summarized, and suggestions for further improvement were put forward.
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Progress of mitochondrial mass control system in the pathogenesis of septic cardiomyopathy

xie you cheng, xiao shu fang, lin xue mei, chen shun, yu xiaohui

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Septic cardiomyopathy (SIC) is a frequently observed organ dysfunction in sepsis, characterized by high mortality and poor prognosis. Understanding the complex pathogenesis of SIC and developing effective therapeutic tools are critical issues that require attention. Previous studies have demonstrated the significant role of mitochondrial dysfunction in the development of SIC. In the presence of SIC and resulting mitochondrial dysfunction, aberrant regulation of the mitochondrial quality control system (MQC) can exacerbate cardiomyocyte injury. Recent studies have demonstrated that the mitochondrial quality control system (MQC) maintains mitochondrial dynamic homeostasis through its regulation of mitochondrial biogenesis, fusion/fission, and autophagy. Consequently, this article provides an overview of the role of MQC in SIC pathogenesis, reviews the latest studies, and analyzes its potential as a therapeutic target.
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Animal Model Analysis of Atherosclerosis Based on Clinical Symptoms in Traditional Chinese Medicine and Western Medicine

Luo Shiwen, Yang Dongmei

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Objectives Based on the clinical characteristics of atherosclerosis in? traditional Chinese medicine (TCM) and Western medicine, this paper analyzes the common animal models of atherosclerosis(AS), and the coincidence of the models with clinical characteristics was scored, in the hope of providing new ideas and reference for studying animal models of AS. Methods This paper reviewed the varieties, modeling methods, modeling principles and characteristics of common animal models of AS. Moreover, according to the clinical diagnostic criteria and symptom characteristics, the similarity of the common animal models was analyzed. Results High-fat feeding type, mechanical injury combined with high-fat feeding type, genetic engineering combined with high-fat feeding type, chemical induction combined with high-fat feeding type and the models of AS combining Chinese clinical syndrome and western disease are widely established in animal models of AS. Comparative analysis result showed that balloon injury combined with high fat feeding type, ApoE receptor knockout mouse combined with high-fat diet type and phlegm and blood stasis type in models of disease and symptom combination showed a comparatively high level of clinical agreement between Chinese and western medicine. Conclusions Presently, most of the animal models of AS had the high degree of coincidence with western medicine, evaluation criterion is dominated by the western medicine as well, which lack of the combination between disease and syndrome, so as to hinder development of concept of Wholism and treatment by differentiation of syndromes in TCM. Therefore, establishing the exact and high coincidence degree animal model, which combines the disease and its TCM symptoms, is the top priority of studying the prevention and treatment of atherosclerosis.
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The role of UBC9 mediated SUMO modification in homocysteine-induced pyrodeath of macrophages

Ma Lingju, Chi Hongyang, Wu xinxue, Ma Fujun, Tian Yancheng, Zhao Caiqi, He Tianyu, Peng hongjian, JiangYideng, Yang Li, Huang Hui, Ma Shengchao

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Objective To study the role of ubiquitin Conjugating Enzyme 9 (UBC9) in the pyrodeath of homocysteine-induced macrophages mediated by SUMO modification. Methods Firstly, The effects of homocysteine at different concentrations (0μmol/L, 50μmol/L, 100μmol/L, 150μmol/L, 200μmol/L) on the viability and pyrodeath of mouse macrophages (RAW264.7) were detected by CCK-8 and Western blot ;Western blot was used to detect the expression levels of UBC9, SUMO-modified protein SUMO-1 and inflammatory cytokine IL-1β in different groups of cells. qRT-PCR was used to detect the mRNA expression of UBC9 before and after interference, and to detect the expression of UBC9, pyrogen-related protein and SUCO-1 after interference.Results After stimulation with 100μmol/L Hcy, the activity of macrophages was not affected, and the expressions of NLRP3 and caspase-1 were the most obvious (P < 0.05).Compared with Control group, the expression levels of and IL-1β were increased in Hcy group (P < 0.01), and the expression of SUMO-1 was increased (P < 0.01). Compared with Control group, UBC9 protein level and mRNA level in Hcy group were increased (P < 0.05). After transfection with si-UBC9, the expressions of NLRP3, caspase-1, IL-1β, UBC9 and SUMO-1 in si-UBC9+Hcy group were decreased compared with si-NC+Hcy group (P < 0.01). Conclusion Hyperhomocysteamine (Hcy) induces pyrodeath in macrophages, and its mechanism is related to the up-regulation of ubiquitin binding enzyme 9 to SUMO modification.
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Visualization Analysis of Research Progress on Neutrophils in Diabetes Based on Citespace

WANG Jin-xi, YU Rong, HUANG Juan, Liu Yangyang, ZHANG Tian-tian, LI Wei, YANG Hui, LEI Shi-hui

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Objective This article aims to clarify the development of neutrophils and diabetes fields, as well as the evolving characteristics, potential trends, and research hotspots of neutrophils in the diabetes field. Methods 2998 relevant literatures on neutrophils in the diabetes field indexed in Web of Science from 2010 to 2023 were retrieved, and visual analysis of the relevant literatures on neutrophils in the diabetes field was conducted using Citespace6.1.R6. Results Since 2012, publications on this topic have grown rapidly. Bayat Mohammad, Liu Tong, Amini Abdollah, Zhang Rui are high-yield authors, with 7 related articles published. China and Shanghai Jiao Tong Univ are the countries and institutions with the most published papers. The most influential journal in this field is "PLOS ONE", cited 1380 times. Literature co-citation analysis shows that the highest focus in topics related to diabetes currently are "extracellular trap" and "covid-19 patient". Co-occurrence analysis, clustering analysis, and keyword burst analysis indicate that "lymphocyte ratio" (13.08) and "neutrophil extracellular trap" (7.2) are the most researched topics in the field of neutrophils and diabetes. Literature in this field mainly focuses on "myocardial infarction", "endothelial", "oxidative stress", and "apoptosis". Conclusion This article analyzes the evolving trends of neutrophils in the diabetes field using Citespace, providing new insights for researchers to conduct future research in the diabetes field.
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Observation on the progress of the murine models of chronic ulcerative colitis induced by dextran sodium sulfate

KONG Weijiao, YAN Yiyue, ZHAO Peikai, MAO Xiaojian, WANG Ting

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Objective To investigate the progress of chronic Ulcerative Colitis (UC) model induced by dextran sulfate (DSS) in mice. Methods 2.5% DSS solution were provided ad libitum for 5 days, and tap water for were supplied for another 5 days in one induction cycle. Male C57BL/6 mice were undergone continuous three cycles of induction to establish the chronic UC model. The weight, disease activity index (DAI), organ index, colon length of mice and pathological changes of colon tissue were determined. The level of myeloperoxidase (MPO) in colon tissue, cytokines such as IL-1β in serum and colon were detected. Results During the three cycles, all mice had diarrhea, bloody stool, weight loss, colon length shortening and pathological injury, which were aggravated after DSS administration and relieved after drinking water administration. The content of MPO in colon gradually increased. The spleen index and the levels of IL-1β, IL-6, IL-17A, TGF-β and TNF-α in serum increased continuously or fluctuating. The contents of IL-1β, IL-6 and IL-17A in colon increased significantly in the first or second cycle, and then decreased slowly. There was no significant change in TNF-α in colon. The concentrations of IL-10 in serum and colon fluctuated up and down, and decreased to a level lower than or remained the same as that in normal group at the end of the experiment. Conclusion Chronic UC model can be successfully induced by 2.5%DSS solution, which is characterized by alternating symptoms of "attack-remission". The persistent systemic inflammatory reaction and overactivation of colonic neutrophils reflect the characteristics of recurrent UC to some extent. It can be used as a tool for analying the pathological changes and interrention opportunities of UC, as well as for discovering and evaluating UC therapeutic drugs.
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Research progress of ferroptosis in sepsis-associated acute lung injury

SHI Yanglin, YANG Jianya, CHANG Qingqing, WANG Qianqian, WANG Minghang, LI Suyun

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Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection, with an extremely high mortality rate. It is the main risk factor for acute lung injury (ALI). However, the pathophysiology and pathogenesis of sepsis-associated ALI are not fully understood, and effective drugs are extremely limited. Therefore, the urgent task is to explore the pathogenesis of sepsis associated ALI and attempt to discover effective intervention measures to improve the prognosis of sepsis associated ALI patients. In recent years, ferroptosis has been considered closely related to the pathological and physiological processes of sepsis associated ALI, and inhibiting related cell ferroptosis can effectively slow down the occurrence and development of the disease. In this paper, the therapeutic strategies targeting ferroptosis of related cells were reviewed, in order to provide reference for the research on ferroptosis of sepsis associated ALI and provide a new perspective for the treatment of sepsis associated ALI.
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Effect and mechanism of ICAM5 on alcohol dependence behavior of mice

Hu Jiajia, Yang Zhuanfang, Sun Xizhe, Yuan Juanjuan, Cheng Yan, Zhang Yu, Yin LITIAN

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【Abstract】 Objective We investigated the effects of ICAM5 in hippocampus of mice alcohol drinking preference, and potential mechanisms. Methods A alcohol two-bottle choice model was developed by 8-week-old male C57BL/6J mice, randomly divided to two groups, the control group and alcohol group. The protein expression of ICAM5 in the hippocampus, amygdala, and medial prefrontal cortex was detected. ICAM5 overexpressed adeno-associated virus was constructed and injected into the hippocampus by stereotaxic method. The expression level of ICAM5 protein in hippocampus was detected by immunofluorescence and Western blot. Then detected the alcohol preference and locomotor activity of mice with the open field test, conditioned place preference experiment, and loss of righting reflex test. Western blot analysis was used to identify neuron F-actin/G-actin ratio. Using Golgi staining, the morphology of dendritic spines was identified. Results In the alcohol two-bottle choice model, the expression of ICAM5 in the hippocampus of mice in the alcohol group was considerably lower than the control group. The specific expression of ICAM5 in the hippocampus of mice was observed by fluorescence microscopy. In the open field experiment, the staying time and moving distance of AAV-ICAM5 group were significantly increased compared with the control group (P < 0.01). In the CPP experiment, the residence time of AAV-ICAM5 mice in the alcohol-paired compartment was significantly lower than that of control mice (P < 0.001). In the lose the righting reflex experiment, overexpression of ICAM5 significantly reduced the sedation latency (P < 0.01), but significantly shortened the duration of sedation (P < 0.001). Compared with the control group, the ratio of F-actin/G-actin in hippocampus was significantly increased after drinking (P < 0.01). But after ICAM5 overexpression, the F-actin/G-actin ratio was significantly decreased (P < 0.001). Compared with the control group, the density of dendritic spines in hippocampal CA1 region was increased after drinking alcohol (P < 0.001), but the density of dendritic spines in AAV-ICAM5+EtOH group was significantly decreased (P < 0.01). Conclusions ICAM5 may modulated the expression of cytoskeleton protein to change structural plasticity of dendritic spines, which contribute to alcohol drinking and locomotor behaviors change of mice.
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Combined with systematic pharmacology and metabonomics to explore the mechanism of baicalein in the treatment of hyperuricemia

liangjingzhen, gaoyingjie, yewenqian, weibingyan, cheenzhaoyang, yangfan

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Objective to explore the effect and mechanism of baicalein in the treatment of hyperuricemia. Methods the mouse model of hyperuricemia was established by yeast extract combined with potassium oxazinate. The effect and potential mechanism of baicalein in the treatment of hyperuricemia were studied by biochemical indexes, pathological changes, non-target metabonomics and network pharmacology. Results baicalein could reduce the contents of uric acid, creatinine and blood urea nitrogen, reduce the inflammatory injury of renal tissue, up-regulate the expression level of uric acid excretion protein and down-regulate the expression level of uric acid reabsorption protein. Nine disease-related targets such as BCL2, SIRT1 and XDH were screened by network pharmacology. Six key metabolic pathways including nicotinic acid and nicotinamide metabolism, caffeine metabolism and purine metabolism were screened by metabonomics analysis. Conclusion baicalein can treat hyperuricemia and reduce renal injury, and its mechanism may be related to the metabolic pathways of nicotinic acid and nicotinamide regulated by SIRT1 and quinolinate.
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Progress in the use of gene editing technologies in the research of immunodeficiency animal models

mayunhui, wangxiaotang, gaojiping, songguohua

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Immunodeficiency animal models play an important role in preclinical research and are important experimental tools in modern biomedical research, widely used in immunology, genetics, oncology and microbiology, and other research fields. Gene editing is a technology of targeted modification of biological genomes, from emergence to application, it has greatly promoted the development of biomedical research. Gene editing technology mainly includes homing endonucleases (HEs), zinc finger nucleases (ZFNs), transcription activator-like effector nucleases (TALENs), and CRISPR/Cas9 systems. At present, researchers has used these technology to establish a variety type of immune deficiency animal models, each with its own advantages and limitation. In recent years, a large number of studies have confirmed that the human immunodeficiency animal model can accurately simulate the function of cancer cells, drugs and immune system in human body, and can better simulate human diseases, and is widely used in the study of human immunobiology and the potential mechanism of human complex diseases. In this paper, we reviewed the progress in the research and application of gene editing technology in the construction of immune deficiency animal models, discussed the problems and optimization strategies of gene editing technology in the preparation of immune deficiency animal models in depth, and prospected its future development prospects, in order to provide references for researchers to select and build immune deficiency animal models.
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Extreme animal protectionism and experimental animal welfare ethics

Tian Xuemei, Sachiko Kubo, Wu Yingjie, Su Tao

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Experimental animals, as "living reagents", promote the development of life science and medicine, and also make the public pay more attention to the welfare ethics of experimental animals. Experimental animal welfare ethics is not only an important part of animal protection, but also plays an important role in protecting the rights and interests of experimental animals and promoting the rationality and morality of scientific research. However, in the evolution of animal protectionism, some extreme theory such as extreme animal protectionism had also emerged. This article summarized the main theories of animal protectionism and the development of animal welfare ethics and analyzed the main problems of extreme animal protectionism. This article expounds the present situation and problems of experimental animal welfare ethics and puts forward some suggestions to promote the practice of experimental animal welfare ethics, in order to provide references for our country's experimental animal welfare ethics practice and system construction.
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Comparative studies of transcriptomics in two murine liver fibrosis models induced by hepatotoxic chemicals

YAN Ruanyu, WU Hongyu, HUANG Kai, SUN Xin, XUE Jingbo, TAO Yanyan, LIU Chenghai, PENG Yuan

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Objective To compare the transcriptomic differences between carbon tetrachloride (CCl4)-induced and Diethyl 1,4-dihydro-2,4,6-trimethyl-3,5-pyridinedicarboxylate (DDC) diet-induced mouse models of liver fibrosis in order to provide a framework for future research utilizing mouse liver fibrosis models. Methods Mouse models of liver fibrosis were induced by 10%CCl4 (2ml/kg) injection and 0.1%DDC diet, respectively. After the 4 -week induction, the serum levels of ALT, AST, and TBil were detected. HE and Sirius red staining were observed to analyze the hepatic inflammation and collagen deposition. Jamall's method was used to evaluate the hydroxyproline (Hyp) content in the liver tissues. Hepatic tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) were measured by the elisa kits. Total RNA was extracted from murine liver tissues for RNA sequencing (RNA-Seq). The differentially expressed genes of the two models were analyzed by R software and then GO and KEGG enrichment were analyzed. Then, cwas used to verify the significantly different genes. Results Compared with normal mice, the serum levels of ALT, AST, TBil and the expressions of hepatic TNF-α, IL-6 and IL-1β were significantly increased in mice received CCl4-induction and DDC diet mice respectively, while the serum level of Alb was decreased. Pathological staining showed that the structures of liver tissues were destroyed and a large number of hepatocytes around the central vein were hyalinized and necrotic in CCl4-treated mice. In DDC diet mice, a lot of porphyrins were deposited in the liver and a large number of inflammatory cells were infiltrated in the portal area and the bile duct. Different degrees of collagen deposition were observed in the liver tissues of the two model mice. Different genes(DEGs) of CCl4-treated and DDC-diet mice were screened according to a filter (|logFC|> 2 times and P < 0.05). 1820 and 2373 DEGs in CCl4-treated and DDC-diet were analyzed, including 1302 and 1978 up-regulated genes , 518 and 395 down-regulated genes, respectively. GO annotation showed that the two models had important functions in molecular function (MF), biological process (BP) and cell component (CC). KEGG analysis showed that 22 and 29 signaling pathways were activated in CCl4-induction and DDC diet model, respectively. Among these, 16 signaling pathways such as extracellular matrix receptor interaction, cell cycle, protein digestion and absorption, focal adhesion, and PI3K-Akt were significantly enriched in the two models (P < 0.05). Cluster analysis showed that Mup11, Mup15, Mup17, Mup1 were significantly down-regulated in both models, which were identified by RT-qPCR (P < 0.05). Conclusions This study reported and compared the RNA-Seq transcriptomic characteristics of liver fibrosis models induced by CCl4-induction and DDC-diet, respectively. By observing the locations of gene expression and the pathways regulated by the genes, an example was established for the subsequent selection of animal models to study the pathogenesis and treatment of liver fibrosis.
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Mechanism of Juanxiao decoction regulating type 3 innate lymphoid cells in treating obese asthmatic mice

TIAN Min ping, ZHANG Qing yuan, XIANG Shuang di, CHENG Ling ling, SUN Peng, XUE Han-rong

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Objective: Explore the mechanism of Juanxiao Decoction in regulating the type 3 innate lymphoid cells (ILC3s) in the treatment of obese asthma. Method: Sixty male BALB/C mice were randomly divided into a normal group, a model group (High Fat Diet+OVA), and Juanxiao Decoction groups (low-, middle-, and high doses of 8.5, 17, and 34 g?kg_-1^{), dexamethasone group (}1 mg?kg_-1^{), with10 in each group.} Except for the normal group, other groups were fed high-fat diet for 12 weeks, and OVA sensitization and atomization inhalation were used to establish an obesity asthma model. From the first atomization, the low-, medium-, and high dose groups of Juanxiao decoction and the dexamethasone group were given corresponding drugs by gavage, while the normal group and model group were given equal amounts of saline by gavage for 7 days. Observing the state of each group of mice and changes in typical symptoms of obesity asthma. Within 24 hours after the last challenge, a fully automated biochemical analyzer was used to detect the four items of blood lipids and the classified count of inflammatory cells in alveolar lavage fluid (BALF). Hematoxylin- eosin (HE) staining was used to observe the morphological changes of lung tissue and abdominal fat in mice. Enzyme linked immunosorbent assay (ELISA) for detecting levels of immunoglobulin E (IgE) in BALF and serum of mice, as well as the levels of interleukin-1β(IL-1β)、Interleukin-13(IL-13)and mouse thymus activation regulating chemokine (CCL17) in lung tissue. The levels of IL-17A₊^{ILC3 and IL-22}_⁺ILC3 cells in lung tissue and peripheral blood of mice were analyzed by flow cytometry. Western blot was used to detect the expression of P-STAT3 protein in lung tissue. Results: Compared with the model group, the general state and typical obese asthma symptoms in the middle and high dose groups of Juanxiao decoction were obviously improved. Pathological staining showed that the airway inflammatory cells infiltrated and the airway wall thickened in the model group. However, compared with the model group, the lung inflammation in dexamethasone group and Juanxiao decoction group was improved, especially in the middle and high dose groups. The levels of IL-1β, IL-17A_⁺ILC3, IL-13 and CCL17 in lung tissue of mice in model group were higher than those in normal group (p＜0.05), while the proportion of IL-22_＋^ILC3 and the expression of P-STAT3 were significantly lower than those in normal group(p <0.01,p＜0.05). After the intervention of middle and high dose of Juanxiao decoction, the levels of IL-1β, 17A₊^ILC3, IL-13 and CCL17 decreased significantly(p＜0.05,p＜0.01,p＜0.001)and the the proportion of IL-22_＋^ILC3 and the expression of P-STAT3 increased significantly(p＜0.05,p＜0.01,p＜0.001).Conclusion: Juanxiao decoction can alleviate lung inflammation and allergic reaction in obese asthmatic mice, and improve the inflammatory environment of the body, and its mechanism may be related to regulating the secretion of cytokines by ILC3.
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Adra1a regulates LPS-induced inflammation in primary hepatocytes of Lbp-/-mice

MI Chuanliang, FU Bin, LI Sidi, CHEN Zhida, GUO Zhongkun, WANG Kezhou

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Objective To Explore the Adra1a regulation of inflammatory response in primary hepatocytes of LBP knockout mice (Lbp-/-) induced by LPS. Method Using two-step perfusion method to extract primary hepatocytes and constracting an primary hepatocyte inflammation model from WT group and Lbp-/- group. Inhibition of Adra1a expression in Lbp-/- mouse primary hepatocytes by adding inhibitor prazosin and transfecting siRNA .The inhibitor method divided the cells into control group (blank control), LPS group (LPS stimulation), and inhibitor piperazine group (LPS stimulation added after 1 hour of prazosin intervention). The method of siRNA transfection divided primary hepatocytes into four groups: control group (blank control), LPS group (LPS stimulation for 12 hours), negative control group (si-NC interference for 12 hours followed by LPS stimulation for 12 hours), and interference group (si-adra1a interference for 12 hours followed by LPS stimulation for 12 hours). The primary hepatocytes of WT mice were divided into two groups: the control group (blank control) and the LPS group (LPS stimulation for 12 hours). This study used WT type and Lbp-/- type mouse primary liver cells as the research subjects to verify the changes of Adra1a under LPS stimulation using Western blot method. Experimental methods such as CCK8, qPCR, and Western blot were used to verify the improvement of inflammation and survival rate of primary liver cells in Lbp-/- mice treated with prazosin and si-adra1a. Results under LPS stimulation, the expression of Adra1a protein in primary hepatocytes of Lbp-/- mice was significantly increased (P < 0.01), while the wild-type did not change; The cell survival rate of the inhibitor prazosin group and the interference group was significantly increased (P < 0.01; P < 0.05); In the inhibitor prazosin group and interference group, the expression of inflammatory factors TNF-α、IL-1β significantly decreased (P < 0.01). The expression levels of proteins p-p38, p-ERK, and p-JNK related to cell damage and inflammation were also significantly reduced (P < 0.01). Conclusion upregulation of Adra1a expression in Lbp -/- mouse primary liver cells induced by LPS compensates for the role of lipopolysaccharide binding protein (LBP) in conducting injury and inflammatory signals, inhibiting the expression of Adra1a gene can significantly reduce the occurrence of inflammation and cell damage in primary liver cells.
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Study on the effect of radiation on mouse salivary gland tissue damage based on NLRP3

wuyuqi, huangguilin, xiaolijun, zhangmin, zhangnini

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Objective: To study the effects of radiation on the morphology, function, and NLRP3 expression of mouse salivary gland tissue, and provide new ideas for repairing radiation-induced damage to salivary gland tissue. Methods: To establish a mouse model of radiation-induced submandibular gland injury and record the weight of drinking water. Salivary flow rate was detected, HE staining was used to observe the submandibular gland injury and Immunohistochemistry and real-time PCR were used to detect the expression of NLRP3 and Caspase-1 in the radiation-induced submandibular gland injury of mice at 1, 3, 7 and 14 days after radiation. Results: With the accumulation of time, the amount of water consumed by the radiation group mice gradually increased, the salivary flow rate decreased, and inflammatory cells in the submandibular gland continued to increase. acinar cells gradually showed lesions such as nuclear pyknosis and vacuolization. At 7 and 14 days after radiation, the expression levels of NLRP3 and Caspase-1 protein and gene in the radiation group were significantly higher than those in the normal group (P < 0.05). Conclusion: Radiation can induce damage to mouse submandibular gland tissue and activate NLRP3 inflammasome to increase its expression level.
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Study on the efficacy of 1470 nm semiconductor laser therapy instrument for canine prostatectomy

HUANG Heng, PAN Yongming, HUANG Junjie, ZHANG Hui, YU Chen, CHEN Minli, XU Qingfeng, ZHENG Guo

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Objective To evaluate the effectiveness of 1470 nm semiconductor laser therapeutic instrument (referred to as curestar therapeutic instrument) for prostatectomy in Beagle dogs. Method 28 adult male Beagle dogs were randomly divided into 3 groups: sham group (n=3), experimental group (n=15), and control group (n=10). The experimental group was further divided into 3 subgroups: 120 W/50 W, 150 W/50 W, and 160 W/50 W for vaporization cutting/coagulation hemostasis, while the control group was divided into 2 subgroups: 120 W/50 W and 150 W/50 W. 5 in each subgroup. Both the experimental group and the control group underwent canine prostatectomy through the entrance of the bladder neck under electrocision. The operational suitability and effectiveness of the product during surgery were observed. After the operation, the general condition of the dogs was observed, and blood biochemical and hematological indicators were measured at before, immediately, 3 days, 7 days, and 28 days after operation. At 1h and 4 weeks after surgery, B-ultrasound and electric resection were performed under anesthesia to observe the condition of the urethra and prostate, and the prostatic tissue was subjected to H&E staining for pathological observation. The thickness of the coagulation layer at 1h after the operation and the repair of the urethelial epithelium at 4 weeks were analyzed. Results During the operation, the experimental and control groups had good operability and showed good vaporization cutting and coagulation hemostasis performance. After the operation, there were no significant effects on the general condition, blood biochemical, and hematological indicators of the dogs. Ultrasound showed that the urethral expansion was visible immediately after the operation, and the echo of the urethral epithelium was slightly enhanced. At 4 weeks, the prostate tissue was slightly low-echo with uniformly distributed small point-like echoes inside, and the capsule was linearly high-echo, consistent with the sham group. The measurement and analysis showed that the weight of the vaporized prostate tissue in the experimental and control groups was about 0.91-1.33 g, with a resection rate of 17.11-20.27 %. And as the power of vaporization cutting increases, the laser emission time gradually decreases, while the vaporization cutting speed and efficiency both increase.However, there was no significant difference between the experimental and control groups (P>0.05). Under the electrocision microscope, a burn-like change was observed in the surgical wounds of the prostate urethra in the experimental group and the control group at 1 h after surgery, and the boundary between the wound and the normal urothelium was clearly visible. At 4 weeks, the urothelium of the prostate had been repaired and flattened, and the boundary with the surrounding normal urothelium was blurred. Similarly, pathological observations also showed that at 1 h after surgery, both the experimental and control groups showed significant damage to the prostate urethral orifice, with a small amount of carbonization and coagulative necrosis on the surface of the wound, a small amount of inflammatory cell infiltration, and a coagulation layer thickness of about 0.4 mm. At 4 weeks, the prostate urethral morphology of the sham group was normal, while the experimental group and the control group both showed new epithelial growth covering the wound, with uniform thickness and no coagulative necrosis tissue attached to the wound. Mild inflammatory reaction was still present in the surrounding area, fibroblast proliferation was obvious, and stromal and epithelial cell proliferation was visible in the surrounding prostate, some of which showed squamous metaplasia. The prostate capsule was intact and the morphology of the surrounding nerves and blood vessels was normal. Conclusion The curestar therapy instrument is effective for prostatectomy in Beagle dogs, with good vaporization cutting and coagulation hemostasis performance, and there was no significant difference in postoperative physiological indicators compared to the sham group.
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Characteristics燼nd營nnovations爄n燛ducation爋f爈aboratory animal science 爄n燭raditional燙hinese燤edicine燙olleges燼nd燯niversities

ZHANG Min, LIU Yanyun, GU Xin, TIAN Daizhi, YANG Yang

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Laboratory animal science plays燼燾rucial爎ole爄n爐he爀ducation燼nd爐raining爋f爉edical爏tudents.燭o爀nsure爐he爀ffective爐eaching爋f爈aboratory animal science爄n燙hinese爉edicine爄nstitutions,爄t爄s爄mperative爐o爄ncorporate爐he爌rinciples爋f燙hinese爉edicine燾haracteristics燼nd爄nnovation.燭his爌edagogical燼pproach燼ims爐o爀nrich爐raditional燾ultural爈iteracy爓ithin燙hinese爉edicine燼nd爁oster爏tudents'燾apacities爁or爄nnovation燼nd燾ritical爐hinking.燭he燿aily爐eaching爋f爈aboratory animal science爏hould爀ncompass爒arious爀ducational燼spects,爄ncluding爄nheritance爀ducation,爀thical爀ducation,爉igration爀ducation,爀xploration爀ducation,爄nspiration爀ducation,燼nd爀xtension爀ducation.燘y爄ntegrating爐hese燾omponents燼nd爀mphasizing爐he爄ntersections爋f燙hinese爉edicine爓ith爈aboratory animal science,爄mportant燼reas爏uch燼s燼nimal爓elfare爄n燙hinese爉edicine爎esearch,爐he燼pplication爋f燙hinese爉edicine爐heories爄n燼nimal爀xperiments,燾onsiderations爁or燼nimal爉odels爄n燙hinese爉edicine,燼nd爐he爏election爋f爀xperimental燼nimal爏pecies,燾an燽e燼ddressed.燗dditionally,爐his燼pproach爌rovides爂uidance爁or爊ew燿evelopment燿irections燼nd燾ultivates爏tudents'爏cientific爎esearch,爄nnovation,燼nd爌ractical燼bilities爀ffectively.燭he爌rimary爋bjective爋f爐his爌rogram爄s爐o爊urture爏cientific爄nnovation燼nd爌ractical燾ompetence燼mong爏tudents爓hile爌rioritizing爐he爏uperior爍uality爋f爄nnovative爀ducation爓ithin爐he燾ontext爋f燙hinese爉edicine.燬uch爀fforts爋ffer燼爏olid爁oundation爁or燼dvancing爄ndigenous爉edical爌ractices燼nd爊urturing燼爊ew爂eneration爋f爌rofessionals燿edicated爐o爌reserving爐raditional爉edicine.
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Effects of acute sleep deprivation on behavior and synaptic biomarker expression in rats at different times

zhangshibin, wang lu, wang chu, guo pengcheng, yan xusheng, huo dongsheng, yang zhanjun, wang yanguo, jia jianxin

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Objective: To investigate the effects of acute sleep deprivation on the behavior and synaptic protein expression in rats at different times. Methods: Seventy healthy male Wistar rats were randomly divided into 7 groups, control group, different time sleep deprivation groups (24 hour, 48 hour, 72 hour, 96 hour, 120 hour and 144 hour). The sleep deprivation rat model was established by modified multi-platform water environment sleep deprivation method. Spatial learning and memory was detected by Morris water maze, anxiety was detected by open field test, and the morphology and quantity of hippocampal neurons were observed by Nissl staining. Western blotting and Real-time PCR determined the expressions of synaptophysin (SYN), post-synaptic density protein-95 (PSD-95) and brain-derived neurotrophic factor (BDNF) in rats. Results: Compared with the control group, the numbers of standing and modification all significantly increased accompanied by the prolongation of sleep deprivation time (P<0.05). The escape latency and path length significantly increased in rats in the 120 h and 144 h groups (P<0.05), while the number of crossing platforms and the percentage of target quadrant time all significantly decreased (P<0.01), and were negatively correlated with sleep deprivation time. The expression levels of BDNF, SYN and PSD-95 all significantly decreased accompanied by the prolongation of sleep deprivation time (P<0.01), and was negatively correlated with sleep deprivation time. Conclusion: With the increase of sleep deprivation time, cognitive dysfunction and anxiety gradually deteriorated, which may be related to decrease in expression level of synaptic biomarkers.
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Exploring the mechanism of Inonotus obliquus extract in treating Crohn?s disease based on proteomics

han lihua, Zhao Xiaoru, Peng Lili, Hao Miao, Yuan Hongxia

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Objectives To investigate the effect of Inonotus obliquus extract on Crohn's disease and its mechanism by proteomics technology. Methods Crohn's disease (CD) model was induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS). A total of 48 SD male rats were randomized into control, model, mesalazine (225 mg/kg), and low-dose (200 mg/kg), medium-dose (400 mg/kg), high-dose (800 mg/kg) Inonotus obliquus groups. The disease activity index (DAI) score and the colonic mucosal injury index (CMDI) score were assessed after one week of drug intervention. HE staining was used to observe the histopathological changes in the colon, and ELISA was used to detect the levels of IL-1β, IL-6, and TNF-α in the blood. Proteins were extracted from the colonic tissues of the control group, model group, and Inonotus obliquus extract high-dose group, and bioinformatics analysis was performed for the proteins identified by quantitative proteomics. Finally, WB and RT-PCR were employed to verify the key proteins. Results The Inonotus obliquus extract improved the symptoms of colitis induced by TNBS in rat, and decrease the levels of IL-1β, IL-6, and TNF-α in the blood. Proteomic tests showed that there were 199 differentially expressed proteins (DEPs) between the Inonotus obliquus extract high-dose group and the model group, of which 63 DEPs were related to CD. Bioinformatics analysis showed that these 63 DEPs were mainly involved in NOD-like receptor signaling pathway, calcium signaling pathway, necroptosis, and other pathways. Consistent with proteomic results, expressions of Vdac1 and Trpv2 were confirmed by WB and RT-PCR in colon tissue. Conclusion Inonotus obliquus extract may regulate NOD-like receptor signaling pathway, calcium signaling pathway, and necroptosis by interfering with the expression of Vdac1 and Trpv2, so as to achieve the effect of treating CD.
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The research progress of traditional Chinese medicine treatment of breast cancer depression and co -disease

PENG Mengwei, WU Yaosong, LIU Gaoyuan, KUANG Luoyi, LUO Zilong, CHEN Yulong, LIU Yan

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Pathological mood changes, mainly depression, occurring during the diagnosis and treatment of breast cancer are clinically called breast cancer related depression(BCRD). A large number of epidemiology and clinical studies have confirmed that BCRD is complex， difficult to treat,and has a poor prognosis. Most of the existing clinical treatments are postoperative chemotherapy for breast cancer and antidepressant drugs, which treats breast cancer and depression as two independent diseases,with many defects such as low efficiency and strong adverse reactions. Traditional Chinese medicine（TCM）has a unique value in the prevention and treatment of breast cancer-related depression by virtue of its significant advantage of regulating multiple pathways and targets with its multiple components at the same time.In this paper,we review the mechanism of BRCD and the therapeutic mechanism of TCM from the aspects of neurological disorders, inflammatory immune response, and intestinal flora disorders, with a view to providing certain references for the clinical application and research of TCM in the treatment of BCRD.
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Study on the therapeutic effect of Qingre Jiedu formula on gout mice based on immune inflammation and intestinal microecology

hexianshun, linkun, weiyurou, tianjiaqing, jiangyulai, weitengfei, lintianye, hemincong, weiqiushi

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Objective: To explore the anti-inflammatory effect of Qingre Jiedu（QRJD） Formula on gout mice and its effect on gut microbiota.Method: Forty 20-22 g C57BL/6 were divided into Control group（CON）, model group（MOD）, allopurinol group（Allo）, QRJD Formula group（QRJD）, and ig 10 g/ 0.1ml carboxymethyl cellulose in blank group every morning from 1 to 28 days. Hyperuricemia mouse model was prepared by potassium oxyazinic acid (500 mg/kg) + yeast extract (10 g/kg) suspension intragaically. On the 29th day, 80ul sterile carboxymethyl cellulose was injected into the left ankle of mice in the CON group under isoflurane anesthesia, and gouty arthritis model was prepared by injecting the same amount of sodium urate solution into the left ankle of mice in the other groups. At the same time, each group was treated with corresponding drugs every day. On the 35th day, samples were taken from mice who had been fasting for 6 hours without water. Blood indexes such as uric acid, creatinine and urea nitrogen were detected. Hematoxylin-eosin staining was performed on ankle joints. The cecum contents of mice were collected and the changes of gut microbiota were detected by 16S rDNA high-throughput sequencing method. Results: ① After 7 days of treatment, compared with MOD group, QRJD formula can effectively reduce the concentrations of blood uric acid (P < 0.001), creatinine (P < 0.001) and urea nitrogen (P < 0.05), and effectively protect renal function; ② The pathological results indicated that compared with the MOD group, HE staining showed that the synovial hyperplasia and inflammatory cell infiltration were reduced in the QRJD formula group after treatment. It was found that the cartilage arrangement of the compound was more orderly than before, the cartilage destruction was less than that of the MOD group, and no matrix loss was observed.③ The immunohistochemical results of ankle joint indicated that IL-10 and TGF-β1 were not significantly increased in CON group and MOD group; Compared with MOD group, the expressions of IL-10 and TGF-β1 of QRJD recipe were increased (P < 0.05).④ In terms of biodiversity, there was no significant difference in α diversity among the four groups (P < 0.05), while β-diversity was found to be more similar to the CON group (P=0.001).⑤Compared to the CON group, the MOD group exhibited increased abundances (P < 0.05) of Ruminococcaceae spp., Dubosiella sp., Tyzzerella sp., Ileibacterium sp.and Bacteroidales spp.In contrast to the MOD group, the QRJD group showed elevated abundances (P < 0.05) of Lactobacillus sp., Ligilactobacillus sp., and Bacteroides sp. Furthermore, the interaction network of the gut microbiota indicated mutual interactions among these microorganisms.⑥In the correlation analysis between gut microbiota and renal function, as well as anti-inflammatory factors, it was observed that the relative abundance of Dubosiella sp., Tyzzerella sp.and Bacteroidales spp. was significantly positively correlated with SUA and SCR (P < 0.05). On the other hand, Lactobacillus sp., Ligilactobacillus sp., and Mitochondria spp. exhibited a positive correlation with anti-inflammatory factors IL-10 and TGF-β1, with a more significant association observed with TGF-β1 (P < 0.05).⑦COG function prediction suggested that the functions of QRJD formula group were concentrated on inorganic ion transport and metabolism, carbohydrate transport and metabolism, etc. Conclusions: QRJD effectively modulates immune inflammation and gut microbiota dysbiosis, thereby treating gout. It is hypothesized that its mechanism of gout prevention and treatment involves the regulation of gut microbiota diversity and abundance, as well as the control of the abundance of differential bacterial species such as Ruminococcaceae spp., Dubosiella sp.and Lactobacillus sp. to achieve the goal of gout therapy.
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Research progress on the involvement of macrophages in myocardial ischemia reperfusion injury mediated by NF-κB signaling pathway

lishilong, wanghe

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Myocardial ischemia reperfusion injury（MIRI）has become one of the most serious complications affecting the clinical outcome of patients with cardiovascular diseases. The immune inflammatory response of macrophages is closely related to the occurrence and development of MIRI.Many studies have shown that the NF-κB signaling pathway can participate in MIRI regulation by influencing the polarization and inflammatory state of macrophages, pyrodeath, infiltration and other functions, and is a potential target for MIRI therapy.Therefore, this article will review the research progress of NF-κB signaling pathway between macrophage function and MIRI regulation.
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Comparison of liver and adrenal orthotopic transplantation models of neuroblastoma

chen Hongxia, Tan Zhigang, Lin Huiran, Feng Luping, Zheng Chuya, Liao Wenfeng, Zeng Rufeng, Liu Jinxin, Zhuo Zhenjian

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【Abstract】Objective The Neuroblastoma (NB) liver transplantation model was established and compared with the adrenal orthotopic transplantation model to explore the characteristics of the model.. Methods 5×105 (SK-N-SH) cells was implanted into the left lobe of mouse liver along the long axis of liver lobe with a micro-injection needle. The growth, metastasis, expression of related genes and histopathological changes of tumor were detected after the modeling. Results The tumor formation rate of mice inoculated with tumor cells reached 100% after 21 days, and the tumor growth, metastasis, related gene expression and pathological characteristics were obvious. Conclusion In this paper, neuroblastoma liver transplantation model was successfully constructed by a relatively simple surgical modeling method, which provides more ideal model choices for future scientific experiments of NB researchers.
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A comparative study of two methods for the clearance of macrophages from the rat endometrium

XIA Liangjun, CUI Chuting, LI Junwei, CHENG Jie, XIA Youbing

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Objectives A comparison of different administration routes of clodronate disodium liposomes to determine which is the most effective method of rat endometrial macrophage clearance. Methods Female 8-week-old SD rats were randomly divided into the unilateral control group (injected 100μL PBS liposomes into the left uterine cavity), unilateral clearance group (injected 100μL clodronate liposomes into the right uterine cavity), bilateral control group (injected 100 μL PBS liposomes into the bilateral intrauterine), bilateral clearance group (injected 100 μL clodronate liposomes into the bilateral intrauterine), and whole-body control group (injected 500 μL PBS liposomes into the caudal vein ) and whole-body clearance group (injected 500 μL clodronate liposomes into the caudal vein). Haematoxylin and eosin (H&E) staining was used to observe the morphology and structure of uterine and ovarian tissues, immunohistochemistry was used to observe the positive presence of macrophages in uterine and ovarian tissues, and flow cytometry was used to detect changes of the macrophages cell counts in uterine and ovarian tissues. Results There was no significant difference in the structure and morphology of the uterus and ovary among all groups. Immunohistochemical staining showed that compared to the control group, the positive expression of uterine macrophages in unilateral and bilateral clearance groups was significantly decreased (P<0.001), and had no effect on the accumulation of macrophages in the ovary (P>0.05). The numbers of macrophages in both uterine and ovarian tissues decreased of whole-body clearance group (P<0.01, P<0.01). Compared with unilateral and bilateral clearance groups, whole-body clearance group had a greater effect on the positive expression of macrophages in ovarian tissues (P<0.05). Flow cytometry showed that compared with the control group, the percentage of macrophages in the uterine tissue was significantly reduced in each clearance group (P<0.001, P<0.001, P<0.05). Compared to the whole-body clearance group, the clearance effect of endometrial macrophages was better in the unilateral and bilateral clearance groups (P<0.05，P<0.05). In addition, the number of macrophages in ovarian tissue decreased in all clearance groups compared to the control group. The decrease in macrophage number was most pronounced in the whole-body clearance group (P<0.05), and there was no statistically significant difference between the unilateral and bilateral clearance groups compared with the control group (P>0.05).
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Effect of Alzheimer"s disease on auditory function in APP/PS1 transgenic mice

GUI Fei, SONG Dan-dan, WANG Hai-yan, SUN Xiao-pin, Yang Lei

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Objective To explore the hearing and cochlear himorphological changes in APP/PS1 transgenic mice during the process of AD, and to determine whether the occurrence and development of AD will affect their hearing function. Methods APP/PS1 transgenic mice and littermates wild type mice were selected at the age of 4, 8 and 12 months. The changes of auditory function in APP/PS1 transgenic mice at different months were detected by immunofluorescence staining and auditory brainstem response (ABR). Results Compared with the control group, the number of Aβ plaques in the hippocampus of 4-month-old APP/PS1 transgenic mice was significantly increased, indicating that AD symptoms were already present at this time. At the age of 4, 8 and 12 months, there was no significant difference in the hearing threshold between APP/PS1 transgenic mice and wild type mice. The histomorphological examination of the cochlea showed that there was no significant difference in the key cells of the inner ear such as cochlear hair cells and spiral ganglion between the two groups of mice. ABR test results of APP/PS1 transgenic mice and littermate wild-type mice showed that the hearing threshold of both mice increased significantly with age, both of them showed age-related hearing loss. Conclusion There is age-related hearing loss in APP/PS1 transgenic mice, but the occurrence and development of AD has little effect on the hearing function of APP/PS1 transgenic mice.
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Improvement of Depressive-like Behavior in Hemerocallis citrina Baroni Using a Zebrafish Model

Zheng Hanwen, Wang ZiHang, Liu Xinyue, Yu Jiawei, Alberto Carlos Pires Dias, Wang Qiong

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Abstract OBJECTIVE: This study aimed to investigate the potential positive effects of the alcoholic extract of Hemerocallis citrina Baroni on depressive behaviors in zebrafish larvae (Danio rerio) induced by reserpine. METHODS: Zebrafish larvae were divided into various groups, which included a control group, a model group, a model group with fluoxetine (a positive drug), a model group with a low dose of HCE (1.5 mg/L), a model group with a medium dose of HCE (3 mg/L), and a model group with a high dose of HCE (4.5 mg/L). Depression-like behaviors were analyzed using sound and light stimulation. RT-qPCR was utilized to investigate the effects of the alcoholic extracts of HCE on depression-related astrocyte markers (GFAP, C3, C4B, EMP-1, S100α-10) as well as the neurotrophic factor (BDNF) and its receptor genes (P75, TrkB). RESULTS: In comparison to the control group, the model group demonstrated significantly shorter movement distance and reduced movement time under sound and light stimulation (P<0.05, P<0.0001). Following the administration of the alcoholic extract of HCE, zebrafish larvae exhibited significantly heightened sensitivity to light and sound stimulation when compared to the model group (P<0.05, P<0.01). Astrocyte marker genes were up-regulated in the zebrafish brain in the model group compared to the control group (P<0.01). However, when the model group was administered with the alcoholic extract, the expression of astrocyte markers was significantly down-regulated compared to the model group (P<0.01). Neurotrophic factor and its receptor genes (BDNF, P75, TrkB) were down-regulated in the zebrafish brain in the model group compared to the control group (P<0.01). However, in the group administered with Brassica campestris alcoholic extract, the expression of BDNF, P75, and TrkB was significantly up-regulated compared to the model group (P<0.001). These findings suggest that the alcoholic extract of HCE suppresses the inflammatory response caused by astrocyte activation and promotes the production of neurotrophic factors and their receptor genes, thereby exerting an ameliorative effect on depression. CONCLUSION: Alcoholic extracts of HCE can improve depression-like behavioral changes induced by reserpine in zebrafish larvae . They reduce the expression of astrocyte markers in the zebrafish brain and promote the production of neurotrophic factors and their receptor genes, playing an antidepressant role.
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Establishment and validation of a liver injury model in mice induced by chronic low-dose exposure to atrazine

ZHU Yu, SU Ying-shi, HE Bao-guo, LIU Xi, QIN Lei

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Objective To establish a model of long-term atrazine (ATR)-induced liver injury in mice and to evaluate the hepatotoxic effects induced by ATR. Methods C57BL/6-N male mice were randomly divided into drinking control group, 1.5mg/L and 150mg/L ATR dose groups. Serum liver function biochemical indexes and inflammatory factors were detected after 35 and 63 d, hepatosomatic ratio was calculated, and histopathology and ultrastructure of the liver were observed. The levels of lipid peroxidation and antioxidant capacity, the activities of major phase I metabolic enzymes and phase II detoxification enzymes, the expression of related proteins in liver tissues were detected. Results Compared with control group, AST/ALT ratio, pro-inflammatory factors CCL2, TNF-α and IL-6, H2O2 content and the activities of metabolic enzymes NCR, CYPb5 and UDPGT in ATR groups had significant changes (P < 0.05). In 150mg/L ATR group, GGT content, MDA level of peroxide and CYP1A2 expression were significantly increased (P < 0.01), while GSH content was significantly decreased (P < 0.05). Moreover, hepatocyte injury and mitochondrial vacuolation were more serious. Conclusions In a mouse model of low-dose ATR- liver injury, both 1.5 mg/L and 150 mg/L atrazine exposure induced liver injury in mice, with 150 mg/L ATR inducing greater metabolic toxicity in the liver after 63 d.
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Research progress on roles of ferroptosis in chemotherapy resistance of leukemia

anlijuan, haozheng

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Chemotherapy resistance in leukemia is an urgent clinical therapeutic challenge. Ferroptosis is a unique mode of cell death driven by iron-dependent phospholipid peroxidation. Since leukemia is characterised by increased oxidative stress and iron overload, it can be hypothesised that leukemia cells are susceptible to ferroptosis, suggesting therapeutic potential. In recent years, ferroptosis has been extensively studied and used in the treatment of various types of leukemia. Several studies have demonstrated the association between the regulatory pathways of ferroptosis and the mechanisms of leukemia drug resistance. The induction of ferroptosis through different pathways can effectively reduce the resistance of various types of leukemia cells to chemotherapeutic drugs, and thus improve the clinical efficacy. This article summarizes the regulatory mechanisms of ferroptosis, analyzes in detail the association between oxidative stress pathways and iron metabolism pathways of ferroptosis and the mechanism of leukemia drug resistance, and compiles the experimental studies and clinical applications of ferroptosis in the treatment of various types of drug-resistant leukemias, with the aim of providing new ideas and directions for the study of ferroptosis and a new strategy to reverse chemotherapy resistance for leukemia patients in the future.
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Analysis on the Construction and Practice of Animal Biosafety Level-3(ABSL-3)Simulated Laboratory

Li Xiaoyan, Lu Xuancheng, Lu Shuangshuang, Wang Jiaqi, Kalibixiati Aimulajiang, Liu Mei, Liu Keliang, Zainawudong·Yushan

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ABSL-3 laboratory is Animal Biosafety Level-3 laboratory where highly pathogenic microorganisms can be done. In recent years, with the continuous emergence of emerging and re-emerging infectious diseases, high-level biosafety laboratories have played an increasingly important role in the hardware support of pathogenic mechanism, drug and vaccine research and development. The demand for ABSL-3 laboratories is increasing year by year. At the same time, there is also an increasing demand for personnel competence of working in ABSL-3 laboratories. The standardization of pre-service training has become an important guarantee to reduce the risk of personnel working in the ABSL-3 laboratory. The systematized, normalized and standardized training work needs to be carried out in a specific place. Simulated laboratory is the best place. Therefore, it is necessary to establish animal biosafety level-3 simulated laboratory and establish scientific and effective operating standards and mechanisms. This paper introduces the design, construction, operation and function of ABSL-3 simulated laboratory.
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Measurement and Comparative Analysis of Blood Physiological and Biochemical Indexes of Spontaneous Type 2 Diabetes Chinese Hamster in the SHANXI MU Colony

yangyuting, yangyichun, weibingyan, wujianqin, zhangruihu, chenzhaoyang

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Objective: Investigate the blood physiological and biochemical changes in the spontaneously developed type 2 diabetes mellitus (T2DM) animal model of the SHANXI MU colony inbred strain established by the research team in the preliminary stage. Methods: A cohort of spontaneously developed T2DM Chinese hamsters and normal hamsters, each comprising 10 individuals at 12 months of age, were selected for the study. Fasting blood samples were collected and analyzed using the Sysmex XT automated hematology analyzer and the Hitachi fully automatic biochemical analyzer to measure and statistically analyze 15 physiological parameters and 16 biochemical indicators in the blood. Results: Compared with the control group, WBC, RBC, PLT, HGB, ALT, AST, GLU, TC, TG and UA in diabetic group were significantly different(P < 0.05). Conclusion: The blood physiological and biochemical indexes of the Chinese hamster spontaneous T2DM model established by the research group in the early stage were detected, and the changes were in line with the trend of human T2DM incidence, which provided basic data for the application and application of the model.
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Progress in the optimization of CRISPR/Cas9 technology for the construction of genetically modified mouse models

wangyu, wuyong, liangchunnan, fanchangfa

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The rise of CRISPR/Cas9 technology has driven the development of various fields of life science. With the continuous deepening of its understanding, people have made multiple improvements and optimizations to adapt to different application scenarios. The optimization of CRISPR/Cas9 technology has also brought many breakthroughs in the production of genetically modified mouse models. This article briefly reviews the development process of CRISPR/Cas9 technology, and summarizes optimization strategies at the level of CRISPR/Cas9 element optimization, construction of conditional knockout/knockin gene modified mouse models, and delivery systems for CRISPR/Cas9 elements and HDR templates. It looks forward to the future development of this technology.
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The correlation of periodontitis and central nervous system inflammation in hypobaric hypoxia environment at plateau

chen lu, jiang xiao xia, zhu ling ling

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In recent years, with the increasing number of people active in the plateau and mountainous areas, high altitude exposure has become increasingly common, and many patients with underlying diseases are affected by the hypobaric hypoxia of the plateau environment, which further aggravates the disease process and even leads to cognitive disorders. Periodontitis is a common inflammatory disease that induces periodontal local inflammatory responses and even causes central nervous system inflammation. At high altitudes, the body suffers from decreased immunity and tissue hypoxia, which can promote the occurrence and development of periodontitis and may even increase the risk of periodontitis leading to central nervous system inflammation. With the deepening of plateau medicine research, the relationship between periodontitis and central nervous system inflammation in the hypobaric hypoxia of plateau environment has attracted more and more attention. This work reviews the research progress of periodontitis and central nervous system inflammation and discusses the correlation between periodontitis and central nervous system inflammation in the hypobaric hypoxia environment at plateau.
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Research progress of exercise on muscular atrophy based on mitochondrial quality Control

GUO Xiaojing, WANG Yan

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Skeletal muscle wasting refers to the loss of skeletal muscle mass and function. Mitochondrial quality control (MQC) is the basis for maintaining normal physiological mitochondrial function, which mainly involves the regulation of mitochondrial biogenesis, mitochondrial dynamics (fission/fusion) and mitophagy. It maintains muscle homeostasis by regulating the relative stability of mitochondrial shape, quantity and quality. As an economical and effective treatment for muscular atrophy, exercise intervention has been widely used, but the relationship between exercise intervention and MQC is not clear. This paper discusses the role of mitochondrial biogenesis, mitochondrial dynamics, and mitophagy in skeletal muscle atrophy and related molecular targets, and thoroughly analyzes the mechanism of MQC-mediated exercise in improving skeletal muscle atrophy caused by aging, disuse, and cancer cachexia, in order to provide theoretical guidance for exercise intervention in skeletal muscle atrophy.
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A comparative study of enzymatic digestion methods for the preparation of single cell suspensions from the lamina propria of the mouse intestine

zengqin, liangying, wangxinhui, yanlei, wangxiangpeng, yangjiayi, yurenhuan

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Objective To investigate the best digestion method for the preparation of single cell suspensions from mouse small intestinal lamina propria. Methods Ten mouse small intestines of uniform length were collected and randomly divided into two groups. Each group prepared the lamina propria single cell suspensions by enzymatic digestion with collagenase A or collagenase VIII, and compared the effects of these two enzymatic digestion methods on the cell yield, cell activity and cell surface antigen of the single cell suspensions, and then the single cell suspensions prepared by the superior enzymatic digestion method were subjected to flow assay. Results Compared to collagenase VIII-based enzymatic digestion, collagenase A-based enzymatic digestion resulted in higher cell yields (9.48 ?1.10) ?109 vs. (4.18 ?1.02) ?109, live cell proportions (86.36 ?3.32) % vs. (61.62 ?10.93) % and active CD45 cells (57.19 ?5.11) ) % vs (26.01?1.44) %, active CD3 cells (8.73?.89) % vs (4.52?.49) %, active CD4 cells (6.19?.09) % vs (3.22?.91) % and active B220 cells (15.06?.27) % vs (5.07?.20) %, providing high quality cells for subsequent flow assays. Conclusion The collagenase A-based enzymatic digestion method is more suitable for the preparation of single cell suspensions from the lamina propria of the mouse small intestine.
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Establishment of chimeric rabbits with FOXN1 gene knockout

liu tian ping, li gui ling, liu ke, chen bang zhu, wang gang, gu wei wang

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Objective The aim of this study was to establish F0 generation chimeric rabbits with FOXN1 gene knockout to explore methods for in vivo conservation of immunodeficient rabbits in a conventional housing environment. Methods Initially, the CRISPR/Cas9 technology was employed to inject the constructed sgRNA and Cas9 protein into a single cell of rabbit two-cell stage embryos to obtain chimeric embryos with FOXN1 gene editing. Subsequently, the embryos were transferred into surrogate does. Finally, the F0 generation offspring were genotyped using PCR and Sanger sequencing, and their growth and development in a conventional housing environment were observed. Results The PCR and Sanger sequencing results confirmed the successful establishment of chimeric rabbits with FOXN1 gene knockout. Observation revealed that the chimeras exhibited normal growth and development in a conventional environment without any immunodeficient phenotypes. Conclusion This study has initially established a chimeric rabbit model with FOXN1 gene knockout, which can grow and develop normally in ordinary environments. This lays the foundation for further breeding of FOXN1 immunodeficient rabbits in the future.
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Characterisation of the immune microenvironment and immunotherapy for cholangiocarcinoma: mechanisms, challenges and prospects

wuxueliang

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Cholangiocarcinoma is a malignant tumour with biliary epithelial features. Currently, early diagnosis of cholangiocarcinoma is difficult and the outcome of treatment is poor. Its microenvironment includes abundant fibrotic mesenchyme and a variety of cell types, and these components promote the development and metastasis of cholangiocarcinoma by interacting with tumour cells through mechanisms such as facilitating migration, suppressing immune response and inducing angiogenesis and lymphangiogenesis. Immunotherapy is one of the important means of current tumour treatment, and immunotherapy for cholangiocarcinoma has made some progress. This article reviews the characteristics of the immune microenvironment of cholangiocarcinoma, its relationship with immunotherapy and cutting-edge therapeutic strategies.
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RANBP9 targeted the expression of TGF-β1 induced the cell apoptosis in colorectal cancer Colo320 Cell

wuxueliang

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objective: To investigate Ran binding protein in microtubule-organization center (RANBP9) targeted the expression of transforming growth factor β1 (TGF-β1) and its effect on colorectal cancer Colo320 cell apoptosis. Methods: The expression data of RANBP9 (gene)? in 625 cases of colon cancer tissues and 20 cases of normal colon tissues in the TCGA database (TCGA) were analyzed. KMPLOT was used to analyze the relationship between the expression of RANBP9 and the survival time of colon cancer patients. The human protein immunohistochemistry database was used to analyze the expression of TGF-β1 in normal colon tissues and colon cancer tissues. The UALCAN database was used to analyze the relationship between the expression of TGF-β1 and the survival of colon cancer patients.The dual luciferase experiment analyzes the relationship between RANBP9 and TGF-β1.The pcDNA3.1-GFP-RANBP9 and pcDNA3.1-GFP-RANBP9-NC were transfected into the cells in the experimental group and the control group,respectively. And the normal group of cells will be established without transfection operation and routinely cultured.MTT method was used to detect the growth viability of each group of cells, flow cytometry was used to detect the apoptotic rate of each group of cells, JC-1 staining was used to detect the mitochondrial membrane potential of each group of cells, and Western blot was used to detect the expression of RANBP9 and TGF-β1 in each group of cells. Results: The expression of RANBP9 in colon cancer tissue was significantly reduced. Compared with patients with low RANBP9 expression, colon cancer patients with high RANBP9 expression had a higher survival curve, and the expression of TGF-β1 in colon cancer tissue was significantly increased. Compared with patients with high TGF-β1 expression, patients with low TGF-β1 expression had a higher survival curve, and the differences were statistically significant (all P<0.05).In colon cancer, RANBP9 can target the expression of TGF-β1. Compared with the normal group, the growth viability of the experimental group, the mitochondrial membrane potential, and the expression of TGF-β1 were significantly down-regulated, and the apoptosis rate and the expression of RANBP9 were significantly increased. The differences were statistically significant (all P<0.05).Conclusion: RANBP9 can target the expression of TGF-β1, promote the growth of colon cancer cell Colo320 and decrease the mitochondrial membrane potential, and induce its apoptosis.
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Hypoglycemic effect of Chinese Yam polysaccharide on DEX-induced IR-3T3-L1 fat cell

LIU Xinyue, WANG Fengzhong, ZHENG Hanwen, Alberto Carlos Pires Dias, FAN Bei, Wang Qiong

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Objective To examine the hypoglycemic effect of Chinese yam polysaccharide on 3T3-L1 insulin resistance cell model. Methods After the creation of the IR-3T3-L1 cell model stimulated by DEX (1 μmol/L). Followed the Chinese yam polysaccharide treatment, the glucose intake and the levels of TC, TG, LDL-C, HDL-C, GSH-Px, MDA, HK and PK were measured. Additionally, the AMPK-PI3K/Akt signaling pathway"s associated genes were identified using qRT-PCR. Results The glucose consumption of IR-3T3-L1 cells was considerably decreased after 48 hours of treatment with 1 μmol/L DEX compared to the control group (P < 0.01), and the reduction persisted for 60 hours. When CYPS at 0.05, 0.15, and 0.45 mg/mL was applied to IR-3T3-L1 cells, the following outcomes were observed: the significantly increased glucose consumption (P < 0.01), HK, PK, GSH-Px enzyme activities (P < 0.01), and HDL-C content (P < 0.01). There was a reduction in the MDA activity (P < 0.01) and the concentrations of TG, LDL-C, and T-CHO (P < 0.01). Additionally, CYPS administration dramatically decreased the levels of PI3K, Akt, GLUT-4, AMPK, IRS-2, PPARa, and Adiponectin mRNA expression (P < 0.05), and reduced the IRS-1, GSK-3β, ACC, and FAS mRNA expression levels (P < 0.01). Conclusions In IR-3T3-L1 cells, CYPS can reduce oxidative stress, control lipid metabolism disorders, and enhance DEX-induced glucose intake. The AMPK-PI3K/Akt signaling pathway"s associated genes may be connected to the process.
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Progress in the study of the mechanism of acupuncture in regulating ferroptosis after ischemic stroke

XUE jing, GAO ying, WANG shu

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Ischemic Stroke(IS)presents a complex pathogenesis,posing numerous challenges in treatment and rehabilitation.Acupuncture, as a traditional Chinese medicine treatment, has garnered widespread attention for its effectiveness in treating IS, particularly in regulating ferroptosis. Ferroptosis is a type of cell death dependent on iron and lipid peroxidation, closely linked to neurological impairment following IS. This article reviews the primary mechanisms of ferroptosis post-IS, emphasizing the interconnections between iron metabolism, lipid peroxidation, mitochondrial damage, and ferroptosis. It further explores the regulatory mechanisms of acupuncture on ferroptosis after IS, including its roles in enhancing mitochondrial function, modulating iron metabolism, alleviating oxidative stress, suppressing inflammatory responses, and influencing various ferroptosis signaling pathways. This aims to provide more scientific evidence and theoretical support for comprehensive therapeutic strategies for IS.
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Effects and comparison of ginsenosides Rg1 and Rb1 depression and anxieti-like behavior induced by chronic unpredictable stress in rats by regulating inflammation

Bei Xueyi, Jiang Ning, Yao Caihong, Zhang Yiwen, Sun Xinran, Luo Yanqin, Li Liang, Xie Mengzhou, Liu Xinmin

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Objective: To study the effect and comparison of ginsenosides Rg1 and Rb1 on depression-like and anxiety-like behavior in chronic unpredictable stress-induced rats by regulating inflammation. Methods: Seventy SPF grade SD male rats were tested for sugar and water preference after 5 days of adaptation. The animals were divided into 7 groups according to the sugar and water preference index, namely blank control group, model group, positive drug group, ginsenoside Rg1 30 μmol/kg dose group, ginsenoside Rg1 60 μmol/kg dose group, ginsenoside Rb1 30 μmol/kg dose group, ginsenoside Rb1 60 μmol/kg dose group. Except for the blank control group, the other rats were randomly subjected to 1-2 different stimulating factors every day for a total of 35 days. On the 36th day, behavioral experiments such as sugar and water preference, open field experiment, novel environment feeding inhibition experiment, elevated cross maze experiment and forced swimming were conducted to investigate its anti-depression and anti-anxiety effects. The serum and hippocampal levels of IL-1β, IL-6, TNF-α and serum corticosterone (CORT) were measured by Elisa. Result: Compared with model group, ginsenoside Rg1 and Rb1treatments significantly increased the sucrose consumption in the sucrose preference test and decrease in immobility in the forced swimming test., the latency to eat in novelty-suppressed feeding test of ginsenoside Rg1 (60 μmol/kg) group was significantly reduced, and percentage of open arm entries and time in elevated plus maze test of ginsenoside Rg1 (30 and 60 μmol/kg) groups was significantly increased. The content of serum corticosterone in ginsenoside Rg1 and Rb1 dose groups was significantly decreased. The levels of serum IL-1β and IL-6 in ginsenoside Rg1 (30 μmol/kg) dose group were significantly decreased, The levels of TNF-α and IL-6 in serum of ginsenoside Rb1 (30 μmol/kg) group were significantly decreased. And the contents of IL-1β, IL-6 and TNF-α in hippocampus of ginsenoside Rg1 and Rb high dose group were significantly decreased. Conclusion: Both ginsenosides can regulate the HPA axis and inhibit neuroinflammation, improving depression and anxieti-like behavior in rats induced by chronic unpredictable stress. In addition, ginsenoside Rg1 has a significantly better anti-anxiety effect than Rb1.
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Gualou Xiebai Baijiu Decoction regulating intestinal microflora and its metabolites to improve atherosclerosis in mice

chenzhifan, chenyulin, niesha, sunwenhao, lichang, mazishan, hukai, heyingying, liuying, tangyaoping

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Objective To explore the mechanism of Gualou Xiebai Baijiu Decoction in improving atherosclerosis (AS) in mice by regulating gut microbiota (GM) and its metabolites. Methous Thirty two male Apoe-/- mice were randomly divided into blank group, model group, atorvastatin(Ato) group and Gualou Xiebai Baijiu Decoction (GXB) group, with 8 mice in each group. Except for the Blank group, three groups of mice were established with AS models and administered by gavage according to their respective groups. Oil red O staining was used to detect the area of aortic plaques. HE staining was used to observe pathological changes in aortic tissue. Using 16S rRNA gene sequencing technology to analyze mouse GM. Detection of mouse GM metabolites trimethylamine oxide (TMAO), short chain fatty acids (SCFA), and serum levels of TG, TC, LDL-C, HDL-C, and NO. Results Compared with the Blank group, both the Model group and Ato group showed an increase in AS plaque area (P<0.05); The serum levels of TG, TC, and LDL-C in the Model group increased (P<0.001), while the levels of HDL-C and NO decreased (P<0.01, P<0.001). Compared with the Model group, the Ato group and GXB group showed a decrease in plaque area (P<0.05); The levels of serum TG, TC, and LDL-C decreased (P<0.001) and the levels of NO were increased (P<0.01) in the Ato and GXB groups; The HDL-C level in the GXB group was increased (P<0.05). Compared with the Ato group, the plaque area in the GXB group was decreased (P<0.05) and the NO level increased (P<0.01).There are 6345 characteristic sequences obtained from 16srRNA. α Diversity analysis suggests that GXB can reduce the richness of GM in AS mice (P<0.001) and improve its uniformity (P<0.05). β Diversity analysis suggests that the microbial community structure of the GXB group is similar to that of the Blank group. There are differences in the abundance of microbial communities among different groups at the phylum and genus levels. At the phylum level, the abundance of Proteobacteria was increased (P<0.01) in mouse AS modeling, while GXB intervention reduced its abundance (P<0.01) and increased the abundance of Verrucomimicrobiota (P<0.05).. At the genus level, GXB intervention can effectively increase the abundance level of Akkermansia (P<0.05). Compared with the Model group, the SCFA level in the GXB group significantly increased (P<0.01), while the TMAO level significantly decreased (P<0.01). Conclusions Gualou Xiebai Baijiu Decoction can regulate intestinal flora and intestinal flora metabolites SCFA, TMAO to improve AS.Akkermansia may be a key bacterial genus for GXB to improve AS through gut microbiota.
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Chronic myocardial ischaemia mouse model of coronary artery disease and evaluation methods

wang zhao bo, panyi, linqian, zhongjuying

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Objective To establish a stable mouse model of chronic myocardial ischemia, and to preliminarily elaborate the electrophysiological principle of T-wave flattening under ischemic state. Methods 1. C57BL/6 J mice were used as control group with normal diet for 3 months. APOE-/- mice were randomly divided into a model group and a Lipid-lowering Drug (LLD) group, and were fed a high-fat diet for 3 months; 2. Plaque condition was assessed by Hematoxylin-eosin staining (HE) and oil red staining; 3. Electrocardiograms of the mice before and after modelling; and 4. Recordings of the ventricular myocytes' action potentials. Results 1. Cholesterol (CHO) and low-density lipoprotein (LDL-C) were significantly elevated in the model group, and lipid plaques appeared in the aorta of the model mice after modelling, while the lesions in the LLD group were significantly reduced, and no plaques were found in the control group; 2. There was no significant change in the T/QRS wave (T/QRS) in the ECG after modelling in the control group, whereas a significant reduction in T/QRS was observed in the model and LLD groups. 3. There was a significant positive correlation between the degree of T/QRS depression and the levels of lipids and the degree of atherosclerosis (AS) pathology. 4. The inner layer of the cardiomyocyte action potential repetitions more slowly than the outer layer of cardiomyocytes, whereas the repetitive rate was accelerated by the ischemic inner layer of cardiomyocytes. cardiomyocytes accelerated the repolarisation rate. Conclusions APOE-/- mice can be used as a mouse model of chronic myocardial ischemia, and the increased repolarisation rate of the inner myocardium in ischemia may be the main reason for the depression of the electrocardiographic "T wave" in ischemia.
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Analysis and reflection on the quarantine and supervision policy of imported experimental animals in Japan

DING Ning, LIANG Jiaqi, FU Hongkun, WANG Ying, ZHU Daozhong, WANG Chunxia, REN Jiao, LIN Zhixiong, TAO Yufeng, MA Lidan, GAO Zhiqiang, WU Xiaowei, Yu haiqiong

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Japan is an important trading partner of China's import and export of experimental animals, and its quarantine supervision policy of experimental animals is meticulous and strict. In this paper, experimental dogs, cats and monkeys are taken as examples to make an in-depth analysis of the regulatory policies of major experimental animals for export to Japan. Through the current experimental animal related laws and regulations, inbound and outbound management measures, experimental animal breeding production and management situation and import and export business trend thinking, from the perfect experimental animal laws and regulations and inbound and outbound management measures, safeguard security, improve the management level of experimental animal breeding and promote experimental animal import and export trade. In order to provide reference for comprehensively improving the level of production, use and management of laboratory animals in China and strengthening the work exchange of laboratory animals between China and Japan.
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Inhibition of gallic acid on lipopolysaccharide-induced inflammatory response in human THP1 macrophages

DIAO Jiawen, XU Hui, MA Xinyue, QUAN Jishu

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Objective To investigate the inhibitory effect of gallic acid (GA) on lipopolysaccharide (LPS)-induced inflammatory responses in human THP1 macrophages. Methods THP1 monocytes were differentiated into macrophages with phorbol myristate acetate (PMA) and then the macrophage inflammation model was established with LPS induction，and GA was given in different concentrations. The safe concentrations of LPS and GA on THP1 cells were screened by CCK-8 method，and the normal group, model group (100 μg/L LPS ) and GA group（100 μg/L LPS + different concentrations of GA）were set up. ELISA was used to detect the levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interleukin-1β(IL-1β) in the cell culture fluid of each group. Microplate method was used to detect LDH activity and NO content in cell cultures of each group, and fluorescence staining was used to detect ROS levels, cell damage and changes in mitochondrial transmembrane potential in each group.Western blotting assay was performed to detect the levels of cyclooxygenase-2 (COX-2), HMGB1,c-Jun amino-terminal kinase (JNK), extracellular-regulated protein kinase (ERK), P38 mitogen-activated protein kinase (P38), nuclear transcription factor-κB (NF-κB), NOD-like receptor protein 3(NLRP3), Caspase-1,IL-1β、Gasdermin D(GSDMD). Results Compared with the normal group, the secretion of IL-6, TNF-α, IL-1β and NO in cell cultures was increased in the model group (P<0.05), and the secretion of COX-2, HMGB1, p-ERK, p-JNK, and p-P38 and p-NF-κB, NLRP3, Caspase-1, IL-1? protein expression was elevated (P<0.05), the expression level of GSDMD protein activation fragment was reduced (P<0.05), ROS generation and cellular damage were significantly increased, mitochondrial transmembrane potential was significantly lower than that of the normal group, and the activity of LDH was elevated (P<0.05); in comparison with the model group, the cell culture fluid of the GA group IL-6, TNF-α, IL-1β and NO secretion were decreased (P<0.05), COX-2, HMGB1, p-ERK, p-JNK and p-P38 and p-NF-κB, NLRP3, Caspase-1, IL-1β protein expression was decreased (P<0.05), GSDMD protein activation fragment expression level was increased (P<0.05), ROS generation and cellular damage were decreased, mitochondrial transmembrane potential was gradually increased, and LDH activity was decreased (P<0.05).Conclusion GAhas an inhibitory effect on LPS-induced inflammatory response in THP1 macrophages, and its anti-inflammatory mechanism may involve MAPK and NF-κB signalingpathways.
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Sanguisorbae Radix alleviates damage in Ulcerative Colitis Mice Based on PPARG and SCL7A11/GPX4

Xiaoxi Yin, Zixuan Chen, Yi Yuan, Jingnan Ma, Jing Wang, Tianyi Lv, Miaomiao Tong, Li Li

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Objective: To investigate the mechanism of Sanguisorbae Radix (SR) in the treatment of Ulcerative Colitis (UC). Methods: The study analyzed GSE92415 from the Gene Expression Omnibus (GEO) database using differentially expressed genes analysis, weighted gene correlation network analysis (WGCNA) and FerrDb. Core genes were identified through protein-protein interaction (PPI) network and correlation analysis. The efficacy of SR in UC was evaluated in a dextran sodium sulphate (DSS)-induced colonic inflammatory mouse model by analyzing DAI, histopathology and colon length. ELISA was used to examine levels of inflammatory cytokines and lipid peroxidation. The expression levels of ZO-1 tight junction protein, PPARG, SLC7A11 and GPX4 protein were examined through Western blotting or immunofluorescence labeling. Results:S Nine differentially expressed genes associated with ferroptosis were screened and PPARG was identified as a key gene. The experimental animal results showed that SR significantly prevented colon shortening and ameliorated histological injuries of colons in DSS-treated mice. SR inhibited cytokine levels of IL-6 and TNF-α, improved the reduction of ZO-1 and levels of MDA and GSH in colon tissues of DSS mice. Meanwhile, it enhanced the activation of PPARG, SLC7A11 and GPX4, which reversed the therapeutic effect of DSS in mice with colitis. Conclusion: Iron death is closely related to UC. SR can inhibit iron death by regulating the PPARG and SCL7A11/GPX4 expression, thereby improving colon epithelial injury and dysfunction in UC mice. This provides ideas and direction for UC treatment strategies.
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Lipidomics driven biomarker discovery in chronic lung disease

Zhang Ang, Liu Xinguang, Du Yan, Xie Yang

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Chronic lung diseases (CLD) include chronic obstructive pulmonary disease, asthma, idiopathic pulmonary fibrosis, etc. Studies have shown that CLD is closely related to the disorder of lipid metabolism. Therefore, lipids, as biomarkers of CLD, may be of great value in the diagnosis, prevention and monitoring of disease treatment.This review mainly discusses four aspects of lipidomics, selection of clinical samples for lipidomics, discovery of biomarkers for CLD, and differentiation of TCM syndromes for CLD.
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Establishment of WHBE rabbit knee osteoarthritis model and intervention study of platelet-rich fibrin releasates

Huang Jun-jie, Chen Min-li, Zhu Ke-yan, Jiang Jing-ao, Zhang Jing-hui, Jiang Chao, Pan Yong-ming

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Objective WHBE rabbit KOA model was established by excision of medial collateral and partial patellar ligaments and intervention with platelet-rich fibrin release solution (PRFr). To investigate the mechanism of cartilage injury and inflammation in WHBE rabbit KOA model and the effect of PRFr intervention on KOA process. Methods Twenty-four WHBE rabbits were randomly divided into three groups: normal control (NC) group (n=6), KOA group (n=12) and PRFr group (n=6). The KOA group and PRFr group injected 0.5 mL of saline and PRFr into both joint cavities on the 7th and 14th postoperative days, respectively. At 4 and 8 weeks of modeling, knee joint grade score, X-ray imaging observation and gross score were performed. Serum levels of IL-1β, TNF-α and MMP-13 were detected by ELISA. Pathological sections were made after decalcification, and then HE staining, toluidine blue staining, safranin o-fast green staining and immunohistochemical expression of TGF-β, BMP3 and NF-κB were detected. Results Lequesne MG behavioral score, Mankin's score and Pelletier score of WHBE rabbits after the operation were significantly increased vs NC group (P<0.01); Pathological observation shows surface defects of cartilage and partial loss of chondrocytes; These results above indicated that the KOA model was established successfully. In KOA rabbits, knee joint swelling, joint pain stimulation and movement limitation were obvious, and X-ray showed high-density soft tissue shadow, indicating more joint effusion, and rough articular surface in general. After PRFr treatment, the levels of serum inflammatory factors (IL-1β, TNF-α, MMP-13) in KOA model rabbits were significantly reversed (P<0.05, P<0.01), and the surface of cartilage became smooth, and most of the chondrocytes were neatly distributed. At the same time, the expression levels of TGF-β, BMP3 and NF-κB induced by KOA were significantly decreased(P<0.01). Conclusion This study successfully established the KOA model of WHBE rabbits, and PRFr can improve the cartilage injury and inflammation of WHBE rabbits KOA model through TGF-β/BMP and NF-κB pathways.
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Potential risks of biosafety and prevention strategies in medical and pharmaceutical research laboratories

Chen Mo, Tao Jiayi, Wang Hongxu, Zhang Qingjian

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Medical and pharmaceutical research laboratory usually involves wide range of study aspects. The materials used in the laboratory are various, including animals, microorganisms and nano-particles and other kinds. Meanwhile, with the production of more and more waste, more biosafety risks would be created. Here, we outlined the potential safety risks related with gene amplification, gene recombination, pathogenic microorganism research, nanotechnology, animal experiments, genetically altered animals, and experimental waste, etc. It also proposed preventive measures for laboratory biosafety risks, which mainly associate with developing strict legal frameworks, bettering hardware infrastructure, strengthening safety awareness, and enhancing education and training programs.
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Research progress on related complications after snake bite

LI Yumei, YANG Yue, YI Jun, YAN Zhangren, WANG Wanchun, DONG Degang

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Snake bite is a common clinical emergency, which has the characteristics of acute onset, rapid changes in condition, high disability and mortality rates. In addition to the common systemic and local tissue damage, snake envenomation can also cause significant complications, including immediate and delayed effects. These complications are also the main causes of disability and even death caused by snake bite, which seriously affect the long-term prognosis and quality of patients’ life. This paper summarizes the symptoms, diagnosis and treatment of snakebite complications from the aspects of blood system, nervous system, motor system, endocrine system, reproductive system and other aspects, in order to provide references for effective and precise treatment of snake bite in clinical practice.
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Research progress of ferroptosis in the mechanism of cerebral ischemia reperfusion injury

jianghuan, BAI Wenya, SHAO Jianlin

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Ferroptosis is a newly cell death mode discovered in recent years, involving in a variety of pathophysiological processes, such as ischemia reperfusion injury, neurodegenerative diseases and tumors, etc. At present, there is a lack of effective methods to prevent and treat ischemic stroke worldwide, and ferroptosis which is involved in cerebral ischemia reperfusion injury. 50 articles were included in this paper after searching the related literature, which published in databases such as PebMed, Wanfang, CNKI and VIP in recent years. Discussing theIorn metabolism and the concept, mechanism and regulation of ferroptosis, the role of ferroptosis in the mechanism of cerebral ischemia reperfusion injury, and the methods of inhibiting ferroptosis, this paper attempts to provide reference for finding a new potential treatment for ischemic stroke from the direction of inhibiting ferroptosis.
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Research progress on MHC function and transgenic mouse models

CAO Xiangwen, LI Min, YIN Qi, HAN Xueliang, WANG Yuan, ZHAO Guangyu

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The major histocompatibility complex (MHC) is closely related to immune regulation, and not only has genetic polymorphisms, but also has species differences in MHC restriction. The construction of humanized MHC transgenic mouse models is an important strategy to break through the differences of MHC species and simulate the characteristics of human immune response. MHC transgenic mice are mainly divided into MHC I or MHC II. single transgenic mouse models and MHC I and MHC II double transgenic mouse models. At present, the strategy of knocking out H-2Kb and H-2Db or knocking out murine β2m is adopted to eliminate the competitive inhibition of HLA I molecules by endogenous H-2 class I molecules, and the construction of HLA II transgenic mouse model is to knock out the β strand of murine origin and transfer it to HLA II. class genes.With the optimization of construction strategies, MHC transgenic mouse models have been applied to epitope vaccine development, tumor treatment, and disease genetic association studies, becoming a powerful tool for preclinical trials. In this paper, we summarize the relevant data of MHC transgenic mouse models, and summarize the construction strategies of MHC transgenic mouse models and their application progress in vaccine development and disease treatment.
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Advances in the study of glucose metabolic reprogramming in the pathogenesis of Alzheimer's disease

Xu Qian, Yang Qiong, Tan Zihu

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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by widespread dementia. Despite extensive research on the pathogenesis of AD over the past fifty years, the underlying mechanisms responsible for AD-related cellular damage and cognitive impairment remain elusive. Currently, multiple studies have confirmed alterations in glucose metabolism patterns within nerve cells in individuals with AD. This metabolic transition plays a crucial role in cell survival and disease progression, even occurring decades before pathological changes and cognitive dysfunction manifest. This article provides an overview of potential mechanisms through which glucose metabolism reprogramming contributes to AD development in various types of nerve cells and brain regions, as well as their interplay, aiming to establish a foundation for further investigation into AD while offering insights and ideas for the development of novel preventive and therapeutic approaches.
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Analysis of animal model of psoriatic arthritis based on the characteristics of Chinese medicine and Western medicine

Shi Yajin, LI Hanbing, LI Genlin, WU Suhui

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Purpose: In recent years, with the incidence of psoriatic arthritis gradually increasing and incurable in China, it has become a major problem in the medical career. Therefore, In this study, we actively explored the pathogenesis of psoriatic arthritis based on the characteristics of Chinese and Western medicine clinical evidence, summarized the currently available animal models and analyzed and evaluated them. Methods: Literature detected in line with this topic was collated and summarized, and the existing models were given an agreement score through the study of the etiology and pathogenesis of psoriatic arthritis in Chinese and Western medicine, the diagnostic criteria of Chinese and Western medicine, and the analysis of the characteristics of the animal models and their degree of agreement with the clinic. Results: This thesis found that the human leukocyte antigen transgenic mouse model, the multiple hybridization transgenic mouse model, and the mannan-induced mouse model had the highest fit scores. Conclusion: Since psoriatic arthritis is mostly seen in Europe, the preparation methods of animal models are mostly imported from abroad, and there are very few animal models prepared with the characteristics of Chinese medicine, therefore, the model agreement scores of western diagnosis are higher than those of Chinese medicine diagnosis as a whole. It is hoped that in the future, we can combine the unique diagnosis and treatment methods of Chinese medicine to further improve the types of animal models of psoriatic arthritis, so as to provide a basis for the construction of more ideal animal models for the treatment of psoriatic arthritis by combining traditional Chinese medicine and Western medicine.
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Research progress of mitochondrial quality control in respiratory diseases

xujingjing

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Respiratory diseases (lung inflammation, pulmonary fibrosis) are a serious threat to human health. As organelles unique to eukaryotic cells, mitochondria not only have important functions in energy production, biosynthesis and maintenance of intracellular homeostasis, but also act as diverse signaling organelles involved in inflammation, proliferation, differentiation, cell repair and other processes. The mitochondrial quality control system includes mitochondrial biogenesis, mitochondrial dynamics, and mitochondrial autophagy. It has been found that certain pathological mechanisms of respiratory diseases such as oxidative stress and inflammation are closely related to dysregulation of mitochondrial quality control. Therefore, this paper summarizes the research progress of mitochondrial quality control dysregulation in respiratory diseases (chronic obstructive pulmonary disease, pulmonary fibrosis, acute lung injury, asthma and bacterial pneumonia), in order to seek new ideas for the prevention and treatment of respiratory diseases from the perspective of mitochondria.
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Neuro-pathological study of the intrathalamic neurovirulence test of poliomyelitis vaccine in rhesus macaques

YU Pin, XU Yan-feng, HAN Yun-lin, ZHAO Wen-jie, QIN Chuan

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Objective To study the effect and pathological mechanisms of the neuro-immune response of viral encephalomyelitis caused by the virulence reversion of the intrathalamic neurovirulence test of poliomyelitis vaccine in rhesus macaques. Methods The stock solution (not less than 7000 lgCCID50?L-1) of the inactivated polio vaccine (Vero cells) of type I, type II and type III Sabin strains and 10-1 dilution of each type of polio vaccine were carried out using intrathalamic neurovirulence test. We observed the pathological changes of polio. Via immunohistochemical method, the distribution of receptor CD155 and CD4+ T lymphocytes, CD20+ B lymphocytes and CD68+ microglia were detected. Results Lesions were observed on the virulence reverted polio case. Inflammatory cells infiltrating, neuronal degeneration and necrosis, satellite phenomenon, perivascular cuffing and glial cell proliferation were observed in the spinal cord. The inflammatory cells were mainly CD4+ T lymphocytes, CD20+ B lymphocytes, and CD68+ microglia in perivascular cuffing and proliferative glial nodules. There is no significant difference on distribution of poliovirus receptor CD155 in neurons and glial cells of monkeys with and without polio, while no expression was observed in vascular endothelial cells. Conclusion Polio caused by virulence reversion of the intrathalamic neurovirulence test is viral encephalomyelitis.
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Effects and mechanism of Five-elements music on the social behavior of offspring from Stress-Injured pregnant rats

WU Yongye, YANG Liping, ZHAO Jiajia, SONG Qi, HOU Junlin, WANG Yaohui, LI Xiaolin

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Objective To investigate the effects and mechanism of Five-element music on the social behavior of Pregnant Children with Allergic Stress during Pregnancy, in order to provide a basis for the early prevention and treatment of clinical fetogenic affective disorders. Methods Forty-five pregnant mice were randomly divided into three groups: a blank group, a model group, and a Five Element Music group. In the model and Five Element Music groups, the model was induced using the bystander electric shock method. Additionally, the Five Element Music group was exposed to Palace Tune Five Element Music daily from 17:00 to 19:00 during pregnancy. On the 19th day of pregnancy, ELISA was employed to assess the levels of adrenocorticotropin (ACTH) and cortisol (CORT) in the serum of pregnant mice in each group for modeling evaluation. The offspring were subsequently grouped with their mother mice and underwent an 8-week-old three-box social experiment to observe social behavior. We utilized the immunofluorescence double-labeling method to detect glutamatergic neuron activity in the mPFC region of the offspring mice. Furthermore, high-performance liquid chromatography was employed to measure the total glutamate (Glu) content in the mPFC region of the offspring mice, while Gorky staining was used to observe changes in dendritic spines of mPFC neurons in the offspring mice.Results Compared to the blank group, the model group exhibited a significant increase in the levels of ACTH and CORT in the serum of pregnant mice, alongside a significant decrease in the social interaction time and social novelty preference index of the offspring mice. Additionally, there was a significant decrease in the activity of glutamate neurons, glutamate content, and neuronal dendritic spines.In contrast, when compared to the model group, the Wuxing Music group demonstrated a reduction in the levels of ACTH and CORT in the serum of pregnant mice, as well as improvements in the social behavior, glutamate neuron activity, glutamate content, and the condition of neuronal dendritic spines in the offspring. Conclusions The intervention of Five-element music effectively ameliorates offspring"s social behavior disorder resulting from prenatal fear stress, with its mechanism potentially linked to enhancing glutamate neuron activity in the mPFC region.
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Immune cell composition analysis of CAST/EiJ mice

LIUQI, HOU Yongzhi, LI Na, ZHANG Jingjing, LU Jiahan, CONG Zhe, ZHU Lin, XUE Jing

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Objective To explore the possible causes of susceptibility to multiple pathogens in CAST/EiJ mice, immune cell phenotypes in the peripheral blood and spleen of CAST/EiJ mice were analyzed to clarify the immune cell composition of CAST/EiJ mice. Methods Classical dendritic cells (cDCs), natural killer (NK) cells, B lymphocytes, T lymphocytes and their subsets in peripheral blood and spleen of CAST/EiJ mice and C57BL/6J mice were detected by flow cytometry using the cell surface markers CD3, CD4, CD8, CD11b, CD11c, CD19, CD27, CD49b and TCRβ. Results There was no significant difference in the proportion of cDCs between CAST/EiJ and C57BL/6J mice, but the cDC1 cell subset was low. The proportion of NK cells (mainly mature NK cell subsets) and T lymphocytes (mainly CD8+ T cells) were both lower in CAST/EiJ mice than in C57BL/6J mice, while the proportion of B cells in CAST/EiJ mice were higher than those in C57BL/6J mice. Conclusion The proportion of NK and T lymphocytes in CAST/EiJ mice was lower than those in C57BL/6J mice.
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Evaluation of an animal model of chronic fatigue syndrome based on data mining

Li Ya-qing, Wang Can, miaomingsan

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Objective To study the application of the animal model of chronic fatigue syndrome, and to provide reference for its animal experimental methods and model improvement. Methods Using "chronic fatigue syndrome, animal model" and "chronic fatigue syndrom, animal model" as search terms, we searched in China Knowledge, Wanfang and PubMed databases. Literature on animal models of chronic fatigue syndrome was compiled from July 2000 to July 2023, and experimental animals, modeling methods, positive drugs, and detection indexes were sorted out, and a database was established for statistics and analysis. Results A total of 155 articles were included; the most experimental animals were male SD rats of SPF grade and 6-8 weeks of age, with weights of 180-220g; the most used mice were male KM mice of 18-22g and 6-8 weeks of age; the most used positive drug was ginseng saponin tablets; the most used modeling method was the method of "forced cold water swimming + chronic restraint"; the most used modeling method was the method of "forced cold water swimming + chronic restraint"; the most used modeling method was the method of "forced cold water swimming + chronic restraint". +The most widely used modeling method is the "forced cold water swimming" method, and the modeling cycle is mostly concentrated in 14 days, and most of them adopt the method of intervention while modeling; the testing indexes are mainly behavioral, which mainly include the exhaustion swimming experiment, the open field experiment, the rat-tail suspension experiment, the Morris water maze experiment, and the observation of the general state of the animals, and the second is the serum biochemical indexes, and the most frequently detected indexes are serum MDA, SOD, TNF-alpha, IOD, and IBP, TNF-α, IL-1β, CORT, IL-2, IFN-γ, ACTH, GSH-Px, IgG, IgA, IL-6, etc. The rest of the indicators were selected according to the research purpose, including the indexes of spleen, thymus, etc., the morphological indicators detected by HE staining and ultrastructural electron microscopy, the immunohistochemistry-related indicators, the CRH and Smilax detected by fluorescence PCR, the CRH, the Smilax, the Smilax, and the Smilax. The mRNA expression indexes of CRH, Smad4, BDNF, CREB, IFN-γ, NRF-1, TFAM, Tlr4, etc., and the protein expression indexes of BDNF, CREB, ERK, Bmal1, Clock, NGF, PGC-1α, SIRT1, Smad4, Caspsae-3, etc., were determined by Western blot method. and other related protein expression indicators. Conclusion At present, the pathogenesis of chronic fatigue syndrome is still unclear, and the animal model is mainly based on the stress modeling method of "forced cold water swimming + chronic restraint", which simulates the physical and mental fatigue state of human beings; there is no uniform regulation on the criteria for the formation of animal models, and the evaluation of the model is based on the application of a variety of behavioral experiments individually or in combination, and the objective evaluation indexes are mostly used to argue the etiology of the disease and evaluate the effectiveness of interventions. The objective evaluation indexes are mostly used to prove the conjecture of etiology and evaluate the effectiveness of interventions; the results of the application of various test indexes show that chronic fatigue syndrome may be related to inflammatory response, neurological dysfunction, and mitochondrial dysfunction, and there may be abnormalities in the pathogenesis of immune function, energy metabolism, cell proliferation, and cell death, which is expected to provide reference for the application of the model, and to provide ideas for the model"s refinement. The excavated content is expected to provide reference for the application of the model and provide ideas for the improvement of the model.
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Application and prospect in experimental animal model of chronic stress

YUE Xiaoqi, Li Yuting, JIANG Miao, ZHAO Zigang, NIU Chunyu

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The effect and mechanism of chronic stress on psychosomatic diseases is a hot topic in the field of stress research. The establishment of animal models to simulate human chronic stress state is of great significance in the principle of stress response, the pathogenesis of related diseases, clinical treatment and drug development. In this paper, the commonly used animal models of chronic stress at home and abroad were reviewed, the classification of stressors, animal selection, model construction, pathological manifestations and evaluation indexes were summarized, and the advantages and disadvantages and application progress of various models were discussed, hoping to provide references for the study of model selection of chronic stress response.
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Technological advances in the study of post-stroke neural loop

Chenyanxi, Xuzhidong, Liutingting, Maliansu, Sunfangling, Wangwen

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Neural loops are formed by interconnections between neurons through synaptic structures, Which are the basic units of information transmission and processing in the brain and play an important role in the regulation of neural functions. After Stroke, the neural connections between the infarcted area and the peri-infarct region and the remote area are damaged, resulting in patients at risk for neurological dysfunction or even disability. However, with advances in detection technology, more and more studies have demonstrated that patients with stroke can produce some functional recovery during the chronic phase, possibly related to the re-establishment of synaptic connections and neural circuits. Therefore, the development of specific technology to identify and manipulate neuronal activity patterns, as well as the use of high temporal and spatial resolution imaging strategies to decipher these neurological processes allows us to understand the whole-brain network dynamics of stroke recovery and the mechanisms by which neural loop reestablishment occurs. Furthermore, we could neurobiologically comprehend the closed-loop relationships that underlie the development of stroke pathology to behavioral outcomes. Current technology for studying neural circuits focus on optogenetics, chemical genetics, in vivo calcium imaging, and functional magnetic resonance imaging technology. This article will introduce the working principles of these four major technologies, focus on summarizing the results of their respective applications in resolving neural remodeling after stroke, and briefly analyze the application scenarios, advantages and disadvantages, and future development trends of each technique. This paper will help clinical and basic researchers to to utilize these technologies in discovering new therapeutic strategies as well as evaluating the effectiveness of rehabilitation strategies.
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Analysis of the Role of Brain Plasticity in Improving Depression by Exercise

Chen Xianghe, LU Pengcheng, SHEN Ziming, LIU Chi, ZENG Xinyu, YIN Rongbin

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The research on the mechanism of depression is currently a focus in the field of neuroscience, degeneration of brain plasticity (decrease in volume, structural degradation, and functional disorder of the hippocampus, PFC, CG, etc.) leads to depression. Exercise is an important means of improving depression. Current research has confirmed the important mechanism of improving the volume, structure, and function of the hippocampus, PFC, CG, etc. in this process, but related research results only focus solely on changes in a certain brain volume or connectivity function, lacking a comprehensive understanding Systematic analysis of the mechanism of improving brain plasticity in exercise antidepressant effects. Therefore, this study aims to explore the role of brain plasticity in the occurrence of depression and the improvement of depression through exercise. This helps to comprehensively understand the role of brain plasticity in the occurrence of depression, and will also provide new ideas for exercise intervention in depression.
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Construction and application of patient-derived pancreatic tumor organoid model

LI Peng, HUANG Minli, TAN Dengxu, ZHANG Caiqin, ZHANG Yongbin, SHI Changhong

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Objective To construct a patient-derived pancreatic tumor organoid (PDO) and evaluate its effectiveness. Methods Collect fresh surgical specimens from pancreatic cancer patients for PDO culture; Compared the pathological and genetic characteristics of the PDO model with the primary tumors; Using the PDO model to evaluate the efficacy of clinical chemotherapy drugs and evaluate the effectiveness of the model. Results A PDO model of pancreatic cancer was successfully established. Histomorphological analysis displayed that the PDO model basically maintained the pathological characteristics of the primary tumor. Whole-exon sequencing showed that both organoids and original tumor tissue remained consistent in the gene mutation type and characteristics. Drug screening tests have exhibited that the PDO model had good sensitivity to gemcitabine and irinotecan. Conclusion A case of pancreatic cancer PDO was successfully constructed, which can reflect the histological and genetic characteristics of the original tumor, and can be used for drug sensitivity experiments in vitro, which proves the effectiveness of PDO model and is expected to imply precision medicine.
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Advances in the study of epigenetic regulatory mechanisms of astrocytes

xu liuqing, zhaopeiyuan, liuxihong, duxiaodan, fangmengyang, yuchenyang, houjunlin

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Astrocytes (AS) are the most abundant glial cells in the central nervous system and are involved in many physiology and pathology processes in the nervous system. Alterations in their phenotype are particularly important for the health of the CNS. Epigenetic mechanisms, including DNA methylation, histone modification, non-coding RNA regulation and chromatin remodeling, are closely linked to alterations in AS proliferation, differentiation, inflammation and other phenotypic features, but how these mechanisms function still needs to be explored and summarized. By reviewing the recent advances in the role of epigenetic mechanisms in AS under different physiological and pathological states, aim to provide new ideas for the understanding and treatment of related diseases.
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Experimental study of ursolic acid to ameliorate pancreatic β-cell injury in type 1 diabetic rats based on the TLR4/NF-κB pathway and Th17/Treg cell balance

songyu, zhangxiaoli, chenhuanhuan, tangcong

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[abstracts] Objective To investigate the effects of ursolic acid (UA) on TLR4/NF-κB signaling pathway and Th17/Treg cells in type 1 diabetes (T1DM) rats. Mmthods The T1DM rat model was prepared by intraperitoneal injection of streptozotocin, and randomly divided into blank (Control group) group, model group (Model group), metformin group (MET group) and UA group. General conditions such as body weight and blood glucose were recorded, and peripheral blood and pancreatic tissues were collected after six weeks of gavage to assess insulin intervention. Immunohistochemistry was used to observe the pathological changes in pancreatic tissues; horseshoe crab reagent was used to detect the changes in serum LPS content; qRT-PCR was used to detect the expression of pancreatic TLR4, MyD88, IκBα, and NF-κB p65 mRNAs, as well as the expression of the transcription factors RORγt and Foxp3 mRNAs; and Western blot was used to detect the expression of pancreatic TLR4, MyD88, IκBα , NF-κB p65 protein expression, and transcription factors RORγt, Foxp3 protein expression; flow cytometry to detect changes in the ratio of peripheral blood Th17, Treg cells; ELISA to detect changes in serum TNF-α, IL-6, IL-1β levels. Results After STZ-induced diabetic rats were treated by gavage for 6 weeks, compared with the Model group, fasting blood glucose (FBG) decreased significantly in both the MET and UA groups, and body weights increased; inflammatory infiltration of pancreatic β-cells was reduced; and the expression of TLR4, MyD88, IκBα, NF-κB p65, RORγt mRNA and protein expression was significantly decreased; LPS content was significantly decreased; IκBα, Foxp3 mRNA and protein expression was significantly increased; Th17/Treg ratio was significantly decreased; and TNF-α, IL-6, and IL-1β content was significantly decreased. Conclusion UA can improve the symptoms of rats by reducing LPS shift, inhibiting TLR4/NF-κB pathway, down-regulating RORγt and up-regulating Foxp3 expression to correct the imbalance of Th17/Treg cell ratio in T1DM rats.
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Effects of Shaoyao Gancao granule on hair growth, behavior and hypothalamic pituitary adrenal axis in mice with alopecia areata

QU Baoquan, LYU Shuying, LIN Wenjun, YANG Dingquan

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Objective To explore the effects of Shaoyao Gancao granule on hair growth, behavior and hypothalamic pituitary adrenal (HPA) axis in mice with alopecia areata (AA). Methods Forty-two C3H/HeJ mice were randomly divided into control, model, Shaoyao Gancao granule, corticotropin-releasing hormone receptor 1 (CRHR1) antagonist, and compound glycyrrhizin tablet (CGT) group. Photography, dermoscopy photography, weight weighing, behavioral measurement were taken, as well as corticotropin releasing hormone (CRH), adrenocorticotropic hormone (ACTH), cortisol, glucocorticoid receptor (GR), and brain derived neurotrophic factor (BDNF) were assessed. Results Compared with the model group, high-dose Shaoyao Gancao granules could improve hair regeneration and weight gain (P<0.05), increase the percentage of total exercise distance and central area exercise distance in the open field experiment (P<0.05), reduce the immobility time in the forced swimming experiment and tail suspension experiment (P<0.05), reduce peripheral blood CRH, ACTH, Cortisol levels (P<0.05), and increase the expression of GR and BDNF in the hippocampus (P<0.05). Conclusions Shaoyao Gancao granule can promote hair growth and improve behavioral performance in mice with AA. The effects may be related to downregulating the levels of CRH, ACTH, and Cortisol, upregulating the expression of GR and BDNF, and inhibiting excessive activation of the HPA axis.
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Advances in the study of CAV1 in digestive tract tumors

Wu Zhihang, Pan Haibang, Tang mingzheng, lixiaofeng, rong yao, cuiyan

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[Abstract] Digestive tract tumour is currently one of the most common types of cancer in the world, including esophageal cancer, gastric cancer, hepatocellular carcinoma, pancreatic cancer and colorectal cancer, etc. Their prognosis is not good and the treatment still needs further improvement. Caveolin-1（CAV1）has a dual regulatory effect in digestive tract tumors, which is both a tumor suppressor and a carcinogen. CAV1 plays an important role in cell proliferation, invasion, metastasis, angiogenesis and drug tolerance of digestive tract tumors, the regulation of CAV1 protein and its related signaling pathways may become one of the strategies for the treatment of digestive tract tumors. Therefore, the review analyzes the relationship between CAV1 and digestive tract tumors in terms of structure, function, expression regulation, regulation of epithelial-mesenchymal transition（EMT）and drug resistance in digestive tract tumors in order to provide new ideas for the diagnosis and treatment of clinical digestive tract tumors.
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Advances of Programmed Cell Death in Post-stroke Cognitive Impairment

sunkexin, xiaoyuqian, wanjun, chenshuying, chenlimin, wangyan, baiyanjie

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Post-stroke cognitive impairment (PSCI) is one of the common complications after stroke, which has a significant impact on the quality of life of stroke patients. However, the pathogenesis has not been fully explained. More and more evidence shows that the mechanism of programmed cell death (PCD) is related to PSCI, including apoptosis, necrotic apoptosis, pyroptosis, generalized apoptosis, PARP-1 dependent cell death and iron death. Therefore, it is crucial to have a clear understanding of various mechanisms of PCD and their relationship with PSCI, and to elucidate the role of PCD in the pathogenesis of diseases. The article reviews six PCD pathways related to PSCI, summarizes their mechanisms of action in PSCI, and elucidates the possible crosstalk between different pathways, in order to provide data basis for clinical targeting of regulatory factors in the PCD pathway for the treatment of PSCI.
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Experimental study on the health hazards of brake pad particles and their main component antimony sulfide respiratory exposure in mice

LI Yanhong, XIU Jinghui, ZHOU Li, GUO Jianguo

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Objective To study the potential harmful effects of brake source particles. Methods Grind the brake pad particles or antimony sulfide particles. Subsequently, the mice were exposed through tracheal perfusion for 1 month to observe pathological changes in in the lungs, heart, and liver, and flow cytometry was used to analyze the changes in peripheral blood macrophages and regulatory T cells (Treg). Results After exposure, there was deposition of foreign substances in the alveolar wall of mice, with obvious infiltration of inflammatory cells around blood vessels, which worsened with increasing exposure concentration. In addition, pathological changes such as vascular inflammation and microthrombosis in the heart, and hepatocyte swelling in the liver were observed. Treg cells in peripheral blood decreased and macrophages increased in the antimony sulfide group and low-dose brake pad particles group, while the proportion of M2-type macrophages decreased. Conclusions Exposure to brake pad particles and their component antimony sulfide particles has varying degrees of toxic effects on the lung, heart, and liver of mice, and has a impact on the immune system, indicating the potential health hazards of brake-derived air pollution.
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Effect of Sanjie Quban Recipe on the Keloid Model of BALB/C Nude Mice and Influence on Transforming Growth Factor-β1

Huang ChuHan, Yang DingQuan, Zhong ShiYi, Wu RuiYing, Yang ZhiShan, Fang HuiJuan, Liu QingWu

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Objective This study aimed to investigate the therapeutic efficacy of the Sanjie Quban Recipe on a keloid nude mice model and its impact on Transforming Growth Factor-β1 (TGF-β1). Methods Keloid tissue after surgical resection was transplanted into the subcutaneous back of healthy SPF BALB/C female nude mice aged 6-8 weeks, and the keloid nude mice model was established. The mice were randomly divided into 3 groups, 5 in each group. They were respectively treated with Sanjie Quban Recipe, Asiaticoside tablet and sterile pure water. After 28 days of continuous gavage, keloid tissue was exfoliated and weighed, HE staining, Masson staining, and immunohistochemical staining (TGF-β1). The difference of keloid weight between the three groups before and after treatment was compared, and the difference of collagen fiber, fibroblast number and TGF-β1 expression between the three groups after treatment was also compared. Results The weight difference of keloid in the Asiaticoside tablet group was greater than that in the control group, and the weight difference before and after keloid treatment was the largest in the Sanjie Quban Fang group compared with the Asiaticoside tablet group and the control group (P < 0.01). Compared with the control group, the collagen fibers in Sanjie Quban Fang group were loose and the number decreased. The number of fibroblasts decreased. The expression of TGF-β1 in Sanjie Quban Formula group was decreased compared with control group (P < 0.01). Conclusion Sanjie Quban Recipe has certain therapeutic effect on keloid, the mechanism may be through reducing the expression of TGF-β1 in keloid tissue, thereby reducing the proliferation of fibroblasts and the synthesis of extracellular matrix. This study provides experimental basis and theoretical basis for the clinical treatment of keloid with Chinese medicine.
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MiR-379-5p inhibits proliferation, invasion and migration of mouse breast cancer 4T1 cells

Song Yanmei, Sun Ningxin, Liu Chen, Song Yifen, Li Hongli, Yin Chonggao

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By investigating the effects of miR-379-5p on the proliferation, invasion and metastasis of mouse breast cancer 4T1 cells, we provide new therapeutic targets for clinical inhibition of breast cancer proliferation, invasion and metastasis. Methods After plasmid transfection, 4T1 cells were utilized to detect the expression of miR-379-5p using real-time fluorescence quantitative polymerase chain reaction (qRT-PCR); 5-ethynyl-2' doxyuridine (5-ethynyl-2'-deoxyuridine, EdU) cell proliferation assay and Transwell assay to detect changes in proliferation and invasion ability of 4T1 cells in each group; Migration ability of 4T1 cells after overexpression and knockdown of miR-379-5p was examined by scratch healing assay; BABL/c mice were used to establish the transplanted tumor model of breast cancer mice, and the tumor growth in vivo after miR-379-5p overexpression was observed.The transplanted tumor model of breast cancer was established in BABL/c mice, and the effects of overexpression of miR-379-5p on tumor growth and the number and size of lung metastases were observed . Results EdU results showed that knockdown of miR-379-5p enhanced the proliferation ability of cells compared with the control group, and miR-379-5p overexpression reduced the capacity of breast cancer cells to proliferate (p<0.05). Transwell and wound healing assays showed that knockdown of miR-379-5p enhanced the invasion and migration ability of breast cancer cells, and overexpression of miR-379-5p significantly inhibited the invasive and migratory ability of cells (p<0.01). In vivo tumorigenesis experiment of BABL/c mice showed that overexpression of miR-379-5p could significantly slow down the growth rate of tumor (p<0.05) and inhibit lung metastasis (p<0.01 ).In vivo experiments demonstrated that overexpression of miR-379-5p significantly slowed tumor growth (p<0.05). Conclusions miR-379-5p plays the role of tumor suppressor gene in breast cancer and inhibits the proliferation, invasion and migration of mouse breast cancer 4T1 cells.
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Study on pathogenesis and animal model building mechanism of ovarian dysfunction

yangzhihui, Hu Yang, Zong Zheng, Sun Xiangming, Song Hui, Chen Yingxiang, Xu Beilei, Zhang Wenjun, Chen Luning, Li Wenlan

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Premature ovarian insufficiency (POI), also known as "ovarian insufficiency", has a high incidence of 1%-5%, and has been on the rise in recent years, which has seriously affected women's physical and mental health and quality of life. At present, the cause and mechanism of POI are still unclear, and the methods and applications of model construction are also confusing, and most models have some shortcomings in pertinence and stability. This also greatly limits the related research and clinical diagnosis and treatment of POI. Therefore, this paper summarizes and discusses the etiology and pathogenesis of POI and the construction of POI animal models, in order to provide more reference for the study of POI etiology and pathogenesis and the selection and construction of models.
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The effect of AIM in inflammatory reaction and lipid metabolism diseases

Zhang Fan, Tian Chun yu, Wang Jingcun, La Xiaojin

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Apoptosis inhibitor of macrophage (AIM), belongs to the group B of scavenger receptor cysteine rich-super family (SRCR-SF). AIM is a soluble protein secreted by macrophages. The expression of this protein is controlled by the liver X receptor (LXR), and it plays an important role in the immune response of the body. AIM, as a secreted protein of macrophages, plays a broad role. It not only inhibits the apoptosis of macrophages, but also participates in the regulation of macrophage polarization. In addition, relevant studies have revealed that AIM is involved in various physiological and pathological processes such as inflammation, obesity, atherosclerosis and cancer; It was used as a biological diagnosis marker for diseases such as tuberculosis, liver cirrhosis and the like; Besides, it can promote lipolysis of adipose cells by inhibiting the activity of fatty acid synthase (FAS), playing an important role in the regulation of lipid homeostasis, lipid metabolism and autoimmune diseases. In this paper, we reviewed the molecular characteristics of AIM and its effects on inflammation, lipid metabolism and other related diseases, showing multiple functional characteristics of AIM to provide the basis for relevant medical research.
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Autophagy and Neurological Diseases

Liang YuYing, Huang Yong, Liu JunSheng, Ou YiLin, Li YiWen, Zhang Rui, Li Zheng, Zhang Zhi Nan

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Autophagy is the main degradation and recycling pathway of abnormal aggregates and damaged organelles in cells, which maintain the normal metabolic balance and material renewal of cells. Autophagy has neuroprotective effects and can affect the functional state of the nervous system by regulating the homeostasis, development, apoptosis and other physiological processes of neurons and glial cells. In recent years, a large number of studies have shown that nervous system diseases are closely related to abnormal autophagy, and inhibition or overactivation of autophagy affects the occurrence and development of depression, neurodegenerative diseases and schizophrenia. Understanding the mechanism of autophagy in nervous system diseases is of great significance for the prevention and treatment of related diseases. This review mainly reviews the current research progress of autophagy and the above diseases of nervous system, in order to provide reference for further research of these diseases.
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Research progress in the effects of Δ9-tetrahydrocannabinol on the blood-brain barrier

Zhang Qianyao, CHENG Hao, HUANG Yi-zhen, TENG Han-xin, ZHANG Yue, ZAHNG Rui-lin

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The psychoactive properties of cannabinoids are well known, and there has been controversy about whether cannabinoids can be used for therapeutic purposes worldwide.Δ9-tetrahydrocannabinol(tetrahidrocannabinol, THC), the main psychoactive substance in cannabis, its neurological mechanism has not been discovered until recently, and its neurological mechanism of action is still not fully understood. The blood-brain barrier(blood-brain barrier, BBB) is a very important barrier structure to protect the brain and is the first line of defense against foreign substances entering the brain. THC's lipophilic nature and its interaction with the endocannabinoid system make it more likely to act on the BBB. In this paper, we review the neurotoxic effects of THC, focusing on the effect and mechanism of THC on the BBB, and provide a theoretical basis for elucidating the neural mechanism of THC.
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Establishment and evaluation of animal model of Varicocele and Erectile dysfunction

lujie, liqunsheng, zhoulei, lidongrun, shenzhennan, lininghua, zhufanyu, chendong, tangwenping, yangwentao

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Objective By surgery inducing Varicocele(VC) in SD rats and Apomorphine Test(APO Test),we screened the rats with Erectile dysfunction(ED) after VC,and explored the method of establishing VC and ED model.Methods Randomly divide 60 rats into control group,sham group,and model group,with 20 rats in each group.Referring to the Turner method,partially ligate the left renal vein to induce left VC.And conduct three APO Tests to screen rats with ED after inducing VC,observe and record the number of erection,genital grooming,and yawning.Measuring the diameter of spermatic vein.Weighing both testises and kidneys.HE staining and observing the pathological changes in the penis and left testis.The success rate of modeling was calculated in the model group.Results 15 out of 20 rats in the model group were successfully established VC and ED model,with a success rate of 75%.After modeling,the diameter of the left spermatic vein in the model group increased significantly and were significantly higher than before-modeling,and the diameter of the right spermatic vein in the model group increased and were higher than before-modeling.The weight of the left testises in the model group significantly decreased compared to the right testises.There was no significant difference between or within groups in the comparison of bilateral kidney weight. In the model group,the number of erections,yawning and genital grooming decreased significantly,and decreased with the time of modeling.The pathological changes of the left testis and penis were significant in the model group.Conclusions Turner method can induce the increase of the diameter of spermatic vein in rats,causing testis injury and weight loss,and APO Test can screen the rats with ED after VC induction.The combination of the two methods is suitable for establishing an animal model with VC and ED status similar to human.
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Establishment and evaluation of hyperuricemia mouse model based on triple method

ni jianyu, bai ningning, liu xianli, gong lihong, shou qiyang

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Objective: To investigate whether a stable and reliable hyperuricemia model can be established in mice with ICR background by triple modeling method (combined with potassium oxazine, hypoxanthine and 30% yeast paste), and to evaluate the modeling method with positive drug febuxoesta. Methods: The hyperuricemia model of ICR mice was established by using potassium oxazine, hypoxanthine and 30% yeast paste diet, respectively, and the serum uric acid, creatinine, xanthine oxidase (XOD), uric acid oxidase (UOX) and other indicators were detected to evaluate the success of hyperuricemia model.Results: The serum uric acid level of ICR mice was not significantly changed by potassium oxazinate alone, which showed an increasing trend but no significant difference with that of 30% yeast paste diet and hypoxanthine combined groups, while the serum uric acid level in triple administration group was significantly increased at 7 days (P<0.01). After 14 days of dynamic monitoring, blood uric acid level of triple dose induced ICR mice peaked at 7 days. Meanwhile, the activity of XOD enzyme was increased, while that of UOX enzyme was decreased (P<0.001). In addition, triple-dose induced hyperuricemia in ICR mice was sensitive to the positive drug febuxoat, with a significant decrease in blood uric acid levels (P<0.001). Conclusion: The hyperuricemia model of ICR mice can be stably induced by triple administration at 7 days.
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Optimization and evaluation of an acute obstructive suppurative cholangitis model in rats

yukui, Liangxiaoqiang, hanmian, zhangjingzhe

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Objective A stable model of acute obstructive suppurative cholangitis in rats was established to detect its pathophysiological indexes and provide a stable and reliable standardized animal model for the study of acute cholangitis and cholestasis.Methods SPF grade male SD rats were selected and the model was constructed by injection of toxoid into the lower bile duct and ligation of the common bile duct, and the changes in body weight, mortality, major indexes of liver function and histopathological changes in the liver were evaluated before and after modeling.Results After modeling, the body weight of rats in the model group decreased significantly; the number of rats died was less; the main indexes of liver function and liver pathology showed obvious changes of cholestasis and liver function damage.Conclusion In this study, a rat acute obstructive suppurative cholangitis model was successfully established, which has the advantages of easy operation, low damage, low mortality and high successful modeling rate, and can provide a standardized experimental animal model for the study of the mechanism of many common diseases and drug development.
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Research progress of pyroptosis in renal ischemia-reperfusion injury

sunhaojie, zhujunlei, liwei, wangsuogang

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Pyroptosis is a programmed cell death mediated by cysteine proteases, which is characterized by mitochondrial participation, inflammasome assembly, plasma membrane perforation, and inflammatory release. As an important mechanism mediating the body's inflammatory response, pyroptosis plays a key role in renal ischemia-reperfusion injury (RIRI). This article reviews the molecular mechanism of pyroptosis, the mechanism of pyroptosis in RIRI and the research progress of therapeutic drugs in recent years, aiming to provide theoretical reference for the early treatment of RIRI.
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Research progress of mitochondria function regulation by TRP channels and its relationship with cardivascular diseases

zhumeiping, zhangshizhong

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TRP channel is a non-selective cation channe. In recent years, a large number of studies have found that TRP channels take participate in variety of cardiovascular diseases, and the study on mitochondrial function regulation by TRP channel and its relationship with cardiovascular diseases has become a research hotspot. Up to date, the relative references are mainly focused on TRPV, TRPM and TRPC channels. This review focuses on above TRP channels in the regulation of mitochondrial function and their relationship with cardiovascular diseases.
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Exploration of mouse model construction of breast cancer complicated with depression induced by using method of 4T1 breast cancer cell line inoculation combined with chronic restraint stress

liu yan, pengmengwei, Liu gaoyuan, Yang Tiezhu, Zhang wenxian, Wuyaosong, Chen Yulong

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【Abstract】Objective To study the core behavioral symptoms, biological indicators and pathological changes of the mouse model construction of breast cancer complicated with depression induced by using method of 4T1 breast cancer cell line inoculation combined with chronic restraint stress (CRS). Methods BABL/c mice were randomly divided into control group, stress group, tumor group and stress combined with tumor group (S T). 4T1 cell lines were inoculated into the underarm of mice in tumor and S T groups. After tumor formation, mice in the stress and S T groups were subjected to CRS for 21 days. Body weight and food intake of each group were monitored during modeling. After the experiment, depression-like behavior of mice in each group was evaluated by sucrose preference test, open field test, elevated plus-maze test, and forced swimming test. After the mice were decapitated, the weight and volume of mouse tumor were measured. Serum tumor markers including carbohydrate antigen (CA199), carcinoembryonic antigen (CEA), vascular endothelial growth factor (VEGF) and related neurotransmitters including 5-hydroxytryptamine (5-HT), norepinephrine (NE) and corticosterone (CORT) were determined by using Elisa method. HE staining was used to observe the histopathological changes of hippocampus and tumor of mice. Results In mice of S T group, the body weight and food intake were significantly decreased, tumor weight and volume were significantly increased, serum tumor markers (CA199, CEA, VEGF) levels were significantly increased, pleasure and desire to explore the new environment were weakened, stress and despair behaviors were significantly increased, serum neurotransmitters 5-HT and NE levels were significantly decreased, and CORT levels were significantly increased. In addition, the cell arrangement of tumor tissue was loose, the interstitial was reduced, the pathological nuclear classification phase was increased, the arrangement and morphology of neurons in the CA3 region of hippocampus were disordered, and the nuclear vacuolation-like changes were obvious. Conclusion The mouse model of breast cancer complicated with depression induced by 4T1 breast cancer cell line inoculation combined with chronic restraint stress showed the dual typical symptoms and biological indicators of breast cancer and depression, which can provide a good model reference for the experimental study of breast cancer complicated with depression.
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Study on the effect of Buyang Huanwu Decoction in reducing oxidative stress and protecting cerebral ischemia-reperfusion injury in rats' blood-brain barrier

maxian

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Objective To explore the mechanism of Buyang Huanwu Decoction (BYHWD) in reducing oxidative stress levels to protect the blood-brain barrier (BBB) in cerebral ischemia/reperfusion injury (CIRI) rats. Methods: Middle cerebral artery occlusion / reperfusion （MCAO/R）model was established by wire embolization method in rats, and PeriCam PSI laser speckle flow imaging system was applied to detect whether the model establishment was successful. The neurological deficits of rats were evaluated by Zea longa score; The histopathological changes in the rat brain were observed by HE staining; The degree of brain edema was detected by dry and wet weight method; The BBB permeability was detected by Evansblue (EB) staining; Ultrastructural changes of BBB were observed by transmission electron microscopy; The levels of ROS, MDA, and SOD activities, which are related to oxidative stress, were detected by kits; The expression levels of MMP-9 were detected by immunohistochemical staining and Western blot; The protein expression levels of Occludin, ZO-1, and Claudin-5 in TJP were determined by double staining of immunofluorescence and Western blot. Results:BYHWD can reduce neurological deficit scores, alleviate the brain histopathological damage, alleviate the disruption of blood-brain barrier structure, prolonged the dense region of tight junction structure, attenuated the edema of the brain in the ischemic side, and reduce the BBB permeability in MCAO / R rats. BYHWD can decrease the levels of ROS and MDA, increase the activity of SOD, decrease the expression levels of matrix metalloproteinase-9 （MMP-9）, and increase the protein expression levels of Occludin, Claudin-5, and ZO-1. Conclusions: BYHWD can increase BBB tight junction protein expression levels, reduce the permeability of the BBB, protect the ultrastructure of the BBB, and reduce brain edema, and its mechanism may be related to the antioxidant stress of BYHWD and inhibition of MMP-9 activation.
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Effects of decoction of Euphorbia fischeriana Steud. and jujuba against breast cancer of different molecular phenotypes via PI3k/Akt pathway

maliwei, YAO Hongyu, CHEN Zhe, NI Shiyu, CHEN Song, LI Jing, LIU Jicheng

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Objective To explore the effect of decoction of Euphorbia fischeriana Steud. and jujuba (DEFSJ) against estrogen receptor (ER) negative (-) and ER positive (+) of breast cancer via PI3k/Akt pathway, and to provide reference for targeted treatment of breast cancer. Methods DEFSJ extract was prepared and analysed by using UHPLC-Triple Quad. DEFSJ containing serum (CS) was prepared by a method of serumal pharmacology. Different concentrations of DEFSJ-CS were applied to (ER-) MDA-MB-453 cells and (ER ) MCF-7 of breast cancer in vitro for 48 h. Flow cytometry was used to detect the distribution of cellular cycle，DNA ladder assay was used to assess the degree of apoptosis，and Western blot was used to detect the expression of PI3k/Akt pathway-related proteins. The expressions of FoxO3a, FoxO1a and Bim mRNA were detected by a real-time quantitative polymerase chain reaction (qrt-PCR) method. Nuclear translocation of FoxO3a protein was detected by a confocal laser microscopy. Results Five batches of the DEFSJ extract were analysed by using UPLC, and the results showed that the preparation technology was feasible and the quality was controllable, ensuring the accuracy of pharmacological experiments results. DEFSJ-CS can block cells in G2/M phase (P<0.05，P<0.01). The cells treated with DEFSJ-CS emerged the typical apoptotic ladder in DNA ladder experiment. Compared with negative control group, DEFSJ-CS can decrease the proteins expression of p-PI3k，p-Akt，p-FoxO3a and p-FoxO1a (P<0.05, P<0.01) and can increase the proteins expression of Bim (P<0.05, P<0.01), and can decrease the mRNAs expression of FoxO3a and FoxO1a (P<0.05, P<0.01) and can increase the mRNA expression of Bim (P<0.05, P<0.01), and can enhance nuclear translocation of FoxO3a protein in the cells. Besides, these datas all showed that DEFSJ-CS had better effect on (ER-) MDA-MB-453 cells than (ER ) MCF-7 cells. Conclusion The regulatory effect of the DEFSJ extract on anti-breast cancer is involves the PI3k/Akt pathway, and the effect is varies with phenotypic differences.
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To explore the effect of Bufei Jianpi Formula on mitochondrial damage of skeletal muscle in COPD rats based on IRS-1/PI3K signaling axis

shentingting, lisuyun, liya, xuanyinshuang, lijingmei, Ligaofeng, hanbingyang

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Objective To explore the effects of Bufei Jianpi Formula (BJF) on mitochondrial damage of skeletal muscle in COPD rats by regulating IRS-1/PI3K signaling axis. Methods 60 SPF SD rats were randomly divided into blank group, model group (COPD stable stage group), BJF group, pioglitazone group (PIO group), BJF PIO group and aminophylline group, with 10 rats per group. The stable COPD rat model was established by the method of smoking and nasal drip (Klebsiella pneumoniae). The samples were taken from the 9th week to the end of the 20th week, and the weight of the rats was measured every week. Routine sections and HE staining were performed on lung tissue and skeletal muscle tissue respectively, and the corresponding pathological changes were observed under light microscope. Lung function of rats was observed by whole body plethysmography (WBP) at week 0, 8 and 20, including tidal volume (VT) and peak expiratory flow, respectively. PEF), 50% tidal volume expiratory flow (EF50). The mRNA expression of IRS-1, Leptin, PGC1-α and PI3K in rat skeletal muscle was detected by qPCR. The expression of PGC-1α, TFAM, IRS-1, PI3K, AKT, p-AKT and Leptin in rat skeletal muscle tissue was detected by WB technique. Results Compared with the Control group, there were a large number of inflammatory cells infiltrated in the alveolar interstitium and bronchus in the Model group, some alveolar walls were broken and fused to form air cavities, and the fibrous network was destroyed. Compared with Model group, the rupture of alveolar wall and destruction of fibroid network were improved in all groups after medication treatment, and the inflammatory cell infiltration in bronchus was reduced, especially in BJF group and Am group. Compared with the Model group, the skeletal muscle pathology of each group after medication treatment could improve the arrangement space, atrophy and fracture of muscle fibers in different degrees, and the cytoplasmic staining of muscle cells was uneven, among which the BJF group had a more significant effect. Compared with Control group, PEF, VT and EF50 in Model group were significantly decreased from week 8 (P<0.01), while PEF and EF50 in BJF, BJF PIO and Am groups were significantly increased (P<0.01). Compared with Control group, mRNA expression levels of IRS-1, PGC1α and PI3K in Model group were significantly decreased(P<0.01), while Leptin mRNA expression level was significantly increased (P<0.01). Compared with Model group, Leptin mRNA expression levels in four medication groups were significantly decreased (P<0.01), while IRS-1 mRNA expression levels in BJF, PIO and BJF PIO groups were significantly increased (P<0.01). The mRNA expression level of PGC-1α in BJF and BJF PIO groups was significantly higher than that in Model group (P<0.01). Compared with Model group, the expression level of PI3K mRNA in BJF, BJF PIO and Am groups was significantly increased (P < 0.01). Compared with Control group, the protein expression levels of PGC-1α, IRS-1 and PI3K in Model group were significantly decreased (P<0.01), while the protein expression level of Leptin was significantly increased (P<0.01). Compared with Model group, the expression level of PGC-1α protein in BJF group was significantly increased (P<0.05), and the expression level of IRS-1 protein in BJF PIO and BJF groups was significantly increased compared with Model group (P<0.05, P<0.01). The expression level of PI3K protein in Am, BJF and BJF PIO groups was significantly higher than that in Model group (P<0.01), especially in BJF PIO group. Compared with Control group, the protein expressions of TFAM and P-Akt in quadriceps femoris tissue of Model group were significantly decreased, while the protein expressions of TFAM and P-Akt were increased in all treatment groups, but there was no statistically significant difference (P>0.05).Conclusion By regulating IRS-1/PI3K signaling axis, Bufei Jiempi can improve the mitochondrial damage of skeletal muscle, increase the expression of mitochondrial coactivator PGC-1α and mitochondrial transcription factor TFAM, enhance mitochondrial biosynthesis, and reduce the pathological damage of lung and skeletal muscle tissue.
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LIMK1 promotes the progression of cervical cancer by up-regulating the ROS/Src pathway

Jia Yajing, Du Naiyi, Zhao Wei, Li Yongping, Liu Yakun

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Abstract: Objective To explore the effect of LIMK1 on the progression of cervical cancer (CC). Methods LIMK1-overexpressed human cervical cancer HeLa cells were constructed and inoculated subcutaneously in nude mice. The tumor volume was observed and the expressions of NOX2, NOX4, p-Src, p-RUNX3, RUNX3, and MMP-9 proteins in the tumor cells were detected by Western blot assay. LIMK1-overexpressed HeLa cells were cultured under 5%O2 and added with antioxidants. The protein expressions of LIMK1, NOX4, p-Src, p-RUNX3, RUNX3, and MMP-9 in the cells were detected by Western blot assay. The cell migration ability was detected by scratch assay. Transwell assay was used to detect cell migration and invasion ability. Monoclonal proliferation assay was used to detect cell proliferation ability. Results The tumor volume of nude mice inoculated with LIMK1-overexpressed HeLa cells increased significantly, and NOX2, NOX4, p-Src, p-RUNX3, and MMP-9 proteins increased, while RUNX3 protein expression decreased. In LIMK1-overexpressed HeLa cells, the protein expressions of LIMK1, NOX4, p-Src, p-RUNX3, and MMP-9 were increased, RUNX3 protein expression was decreased, while the cell migration, invasion, and proliferation ability were increased. However, after adding antioxidants, the expression levels of NOX4, p-Src, p-RUNX3, RUNX3, and MMP-9 proteins, and the ability of cell migration, invasion, and proliferation were not different from those of HeLa cells with normal expression of LIMK1. Conclusion LIMK1 promotes the progression of cervical cancer by promoting the ROS/Src pathway, thereby promoting the migration, invasion, and proliferation ability of cervical cancer cells.
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Research progress of SHP2 in digestive system tumors

WANG Peng, FAN Jianchun, JIA Juming, DIAO Qingfei, WU Xueliang, Xue Jun

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【Abstract】 Currently malignant tumors have become one of the major diseases threatening human health,with disability and mortality rates increasing year by year.Protein tyrosine phosphatase 2 (SHP2) of Src homology 2, an important member of the PTP family, is a tyrosine phosphatase with a wide range of functions,whose expression is elevated in a wide range of solid tumors,and plays a important regulatory role in invasion,metastasis,proliferation,apoptosis and drug resistance.A large number of studies have shown that SHP2 plays a very important role in the genesis and development of many solid tumors,but there is no systematic report on the role of SHP2 in digestive system tumors.Based on this paper,we reviewed the biological functions and clinical significance of SHP2 in seven different tumors of the digestive system,explored its roles and mechanisms in different cancer development stages,and summarized and looked forward to the development of SHP2 inhibitors,to further search for potential targets for effective early diagnosis and gene therapy,which is of great significance for the improvement of cancer patients' survival rate.
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Research progress on the relationship between regulatory cell death and Dilated cardiomyopathy

QiuYueqing, WangZhentao

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Dilated cardiomyopathy (DCM) is one of the common primary diseases of heart failure and arrhythmias. With the continuous deepening of research in recent years, the intrinsic molecular mechanism of regulatory cell death (RCD) has gradually become clear. Researchers have found that RCD plays a very important role in the occurrence and development of DCM. RCD mainly includes apoptosis, necrotic apoptosis, Pyroptosis, Ferroptosis, autophagy, etc. They have certain correlation and can interact and regulate each other. This article provides an overview of the current research status on the mechanisms of the five RCD modes involved in DCM, in order to provide reference for future related experiments and clinical studies.
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Research progress on the interaction between gut microbiota and microRNA in inflammatory bowel disease

KONG Binghui, BAI Longzhou, YANG Li

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Inflammatory bowel disease (IBD) is a chronic intestinal disorder characterized by an immune response to factors in the intestinal environment. Dysregulation of the intestinal flora may lead to the development of inflammation. Studies suggest that fecal transplants, probiotics, prebiotics, and dietary interventions may play a potential role in reshaping the intestinal flora and treating the disease. MicroRNAs (miRNAs) participate in physiological processes, including cell development, proliferation, and apoptosis. In addition, miRNAs are important in inflammatory processes and play a role in regulating pro- and anti-inflammatory pathways. MiRNA profiles may serve as a diagnostic tool for IBD and prognostic markers for the disease. The relationship between miRNAs and intestinal flora has not been fully elucidated, and recent studies have demonstrated their roles in regulating the intestinal flora and inducing ecological dysbiosis. In turn, the flora can regulate miRNA expression and improve intestinal homeostasis. It is important to continue exploring this relationship. Therefore, the purpose of this review is to analyze the relationship between gut microbiota and miRNAs in IBD and identify possible precision-targeted therapies for IBD.
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Study on the effects of various herbs and different proportions of herbs in Huidu Yinhua Powder on methicillin-resistant Staphylococcus aureus

LI Yufen, JIANG Shuang, SONG Wu, JIANG Tao, LIU Chang, ZHOU Haofang, TANG Yating, SU Xin

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Objective: To study the inhibitory ability of Huidu Yinhua Powder, from “Orthodox Manual of External Medicine”, on methicillin?resistant staphylococcus aureus (MRSA) as well as the inhibitory effect of virulence factor α-hemolysin (Hla) activity and biofilm formation, and at the same time, to explore the optimal ratios of Huidu Yinhua Powder, to provide experimental support for the new use of the ancient formula. Methods: The inhibitory effects of Huidu Yinhua Powder and the herbs in the formula on USA300 were analyzed by minimum inhibitory concentration (MIC), minimum bactericidal concentration (MBC), and disk diffusion assay (K-B method). Hemolysis assay, neutralization assay, Oligomerization assay, Western Blot (WB) to verify in which form the drug inhibits the activity of the virulence factor alpha-hemolysin (Hla). The biofilm assay was performed to evaluate the inhibitory effect of Huidu Yinhua Powder on biofilm, while finally orthogonal experiments were performed to explore the optimal ratios of Huidu Yinhua Powder. Results: Huidu Yinhua Powder inhibited the MRSA strain with a MIC₉₀ of 64 mg/mL and an MBC of 256 mg/mL, with antibacterial circle diameter of 7.50±0.50 mm. Huidu Yinhua Powder inhibits Hla activity by inhibiting Hla secretion and the minimum effective concentration (MEC) was 16 mg/mL, while the MEC of biofilm was 8 mg/mL. In Huidu Yinhua Powder, Honeysuckle and Astragalus only affected the hemolytic activity of MRSA and the formation of biofilm without inhibiting the growth of bacteria, the hemolytic activity MEC and the biofilm MEC of both of them were 32 mg/mL. Glycyrrhiza had a strong bacterial inhibitory capacity, with a MIC₉₀ of 8 mg/mL and a biofilm MEC of 1 mg/mL, without showing inhibitory hemolytic activity at subinhibitory concentrations. The final orthogonal experiment showed that when the ratio of honeysuckle: astragalus: glycyrrhiza in Huidu yinhua Powder was 1:2:4, the MIC₉₀ was 16 mg/mL, the hemolytic activity MEC was 8 mg/mL, and the biofilm MEC was 4 mg/mL, all of which were the lowest among the nine groups. Conclusion: Huidu Yinhua Powder affects the hemolytic activity and biofilm formation of MRSA at sub inhibitory concentrations, with the optimal ratio of honeysuckle, astragalus, and glycyrrhiza being 1:2:4.
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Effect of vitamin D on the structure and diversity of intestinal flora in spontaneously diabetic rats

chen lin, tan hong xing, hao li ping, li yan yan

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[Abstract] Objective To investigate the effect of vitamin D (VD) on intestinal flora in spontaneously diabetic rats. Methods Zucker diabetic fatty rats (ZDF rats) were randomly divided into control group (Con), VD control group (VD), model group (T2DM) and VD intervention group (VD+T2DM). Fasting blood glucose profile and oral glucose tolerance level were detected in rats in each group. The 16S rDNA sequencing technology was used to detect the changes in rat intestinal flora, and OTU analysis (Venn diagram), Alpha diversity analysis (chao1, observed species, PD whole tree, shannon and simpson), Beta diversity analysis [principal coordinate analysis (PCoA)], flora structure and colony species variability analysis [linear discriminant analysis and influence factor (LEfSe) analysis]. Results VD intervention significantly improved fasting blood glucose levels and insulin resistance in T2DM rats (P<0.05).Alpha diversity results showed no significant differences in chao1, observed species, PD whole tree, shannon and simpson indices between T2DM and VD+T2DM groups (P>0.05) ; Beta diversity analysis showed that the VD+T2DM group had more species similarity with the Con group compared with the T2DM group. The dominant bacteria of rat intestinal flora in each group were significantly different; compared with the T2DM group, the VD+T2DM group showed decreased abundance of Bacteroidetes and increased abundance of Firmicutes and Clostridium XIVa. Conclusion VD improved fasting glucose elevation and insulin resistance in T2DM rats; VD improved the structure of intestinal flora, decreased Bacteroidetes, and elevated Firmicutes and Clostridium XIVa abundance in T2DM rats.
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Overview of in vitro skin models of transdermal drug delivery system

LiuYan, HuXiaolei, XuKeHong, ZhaoHaiRong, WuXiuMei, YangZiZhong, ZhangChengGui, ZhaoYu, GaoPengFei

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Skin modeling of transdermal drug delivery systems refers to the experimental models which can mimic the structure and function of human skin to explore and evaluate the absorption, penetration and efficacy of medicines in transdermal drug delivery. It provides alternative to traditional human skin experiments and reducing the utility of human skin in medicines research, which is convenient, controllable, and cost-effective . For the skin models of transdermal drug delivery systems, this paper introduces commonly used animal skin models, artificial skin models, and recombinant human skin models from the perspective of the transdermal absorption pathway of medicines, and analyzes its advantages and disadvantages as well as its applications, so as to provide references for the research and development of transdermal formulations and topical therapies and so on.
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AMPK: Diverse Regulatory Mechanisms and New Perspectives for Disease Treatment

Ning Jinghua, zhang xin, zhang Yuzhe

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The AMP-activated protein kinase (AMPK) is a conserved cellular energy Adenosine monophosphate, plays an important role in regulating cell growth, proliferation, differentiation, autophagy, phosphorylation, crosstalk, and glucose and lipid metabolism. AMPK is activated when the body is low in energy or under certain extreme conditions, and it's suppressed when there's an excess of nutrients to maintain the energy balance. In addition, the regulatory mechanism of AMPK signaling pathway mediating ferroptosis also reflects its unique role. AMPK plays a special regulatory function in different organelles, which provides a new direction for disease therapy. It is also a therapeutic target for the prevention of diseases such as reproductive system diseases, aging, cancer, inflammation and cardiac dysfunction. This article reviews the damage of cellular energy imbalance to the body's microenvironment. AMPK stimulates its potential therapeutic potential in diseases and drugs through diverse signal regulatory mechanisms, it provides a new way of treatment for different system diseases. This review summarizes the diverse regulatory mechanisms of AMPK signaling pathway, and provides theoretical reference for cancer therapy and other diseases therapy targeting AMPK.
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Discussion on the Mechanism of "Brain-Spleen Inflammation Coupling" in Rat Model of Acute Ischemic Stroke Stasis Toxin Syndrome

dongyilei, Liu Yue, Li Junyuan, Fu Jianhua, Zhang Yunling, Yao Mingjiang

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【Abstract】Objective: To investigate the correlation between brain injury and spleen damage in rat models of acute ischemic stroke and stasis interaction, and its effect on the signal axis of MCP-1/CCR2 chemokine, and to provide experimental basis for the mechanism of "brain-spleen inflammatory coupling" in spleen lesions caused by acute ischemic stroke. Methods: Forty male SD rats were randomly divided into sham group, carrageenan/yeast stasis syndrome group (Carrageenan/Yeast, CA/Y), middle cerebral artery occlusion group (MCAO), middle cerebral artery occlusion (MCAO), middle cerebral artery stasis syndrome group (MCAO CA/Y), 10 rats in each group. The CA/Y group and the MCAO CA/Y group were injected with 10 mg穔g-1 carrageenan, 10 mg穔g-1 intraperitoneally on the first day of molding, and 2 mg穔g-1 of dry yeast suspension were injected subcutaneously on the second day, and the MCAO group and MCAO CA/Y group were established by wire embolism on the second day. 24 h after cerebral infarction model, the neurological deficit score was performed on each group of rats, the percentage of cerebral infarction area was observed by TTC staining, the spleen weight was determined, and the correlation between the percentage of cerebral infarction area and spleen weight was further analyzed by Spearman correlation coefficient, the pathological morphology of brain tissue and spleen tissue was observed by hematoxylin-eosin (HE) staining, and monocyte-1 (monocyte) was detected in rat plasma by enzyme-linked immunosorbent assay (ELISA). chemotactic protein 1, MCP-1), interferon-γ γ (IFN-γ) content, western blot method to detect ischemic side brain tissue chemokine C-C-motif receptor 2 (CCR2) protein expression. Results: Compared with the ham group, the neurological deficit score, cerebral infarction area, MCP-1 and IFN-γ content in plasma were significantly increased (P<0.01), spleen weight decreased significantly (P<0.01), and the expression of CCR2 protein in brain tissue was also significantly up-regulated (P<0.05) in the MCAO group and the MCAO CA/Y group. The area of cerebral infarction increased significantly (P<0.01), the weight of the spleen decreased significantly (P<0.01), and the expression of CCR2 protein in brain tissue and spleen tissue was also significantly up-regulated (P<0.05), compared with the MCAO group, the area of cerebral infarction in the MCAO CA/Y group was significantly increased (P<0.01) and the weight of the spleen decreased significantly (P<0.05). Spearman correlation analysis showed that spleen weight was negatively correlated with the percentage of cerebral infarction area (P<0.01, r=-0.9711). The pathological morphological observation results showed that the pathological changes in the MCAO CA/Y group were the most serious, cerebral liquefaction necrosis foci could be seen in the brain tissue cortex, the arrangement of neuronal cells in the lesions was sparse, disordered, volume atrophy, a small number of vacuoles and nuclear solidification, most of the neuronal cells were red degeneration and necrosis, microglia hyperplasia was obvious, small blood vessels were significantly increased, and interstitial lipid degeneration was superb; The density of periarterial lymph sheath cells in part of the spleen tissue is reduced, and the marginal area is widened. Conclusion: A correlation between brain and spleen injury could be found after acute ischemic stroke with stasis and toxins syndrome, and the chemokine signaling axis of MCP-1/CCR2 might be involved in the mechanism of "brain-spleen inflammation coupling".
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Effect of lidocaine regulating Hippo-YAP signal pathway on ischemia-reperfusion injury in orthotopic liver transplantation rats

Liu Yue, Akbar Nurmaimaiti, Ye Jian-rong

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Objective: To explore the effect of lidocaine (LID) on ischemia-reperfusion injury in orthotopic liver transplantation (OLT) rats and to analyze its mechanism of action. Methods: 60 rats were randomly divided into control group, model group, low-dose LID group, medium-dose LID group, high-dose LID group, and Verteporfin group, with 10 rats in each group, except for the control group, and other rats were used to construct OLT models. The pathological changes in liver tissue was observed by hematoxylin-eosin (HE) staining, the serum aspartate transaminase (AST), alanine transaminase (ALT), total bilirubin (TBIL) and lactate dehydrogenase (LDH) activities were detected by automatic biochemical analyzer, the liver tissue inflammatory factor tumor necrosis factor-α (TNF-α), interleukin (IL) -6, IL-1β and IL-10 levels were detected by enzyme-linked immunosorbent assay (ELISA), the reactive oxygen species (ROS) was detected by fluorescence probe method, the malondialdehyde (MDA) was detected by thiobarbituric acid colorimetric method, the superoxide dismutase (SOD) was detected by nitrogen blue tetrazole colorimetry, the glutathione peroxidase (GSH-Px) was detected by spectrophotometer method, the apoptosis of liver histiocyte was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) , and the expression of mammalian STE20 like protein kinase (MST1), phosphorylation (p) - MST1, large tumor suppressor factor 1 (LATS1), p-LATS1, Yes associated protein (YAP), p-YAP, as well as apoptosis related proteins B-cell lymphoma 2 (Bcl-2) and Bcl-2 related X protein (Bax) were detected by western blotting (WB). Results: Compared with control group, the liver tissue in model group rats showed injury, liver cells necrosis and a large number of inflammatory cells infiltration, the cell apoptosis rate, serum AST, ALT, TBIL, LDH activity, liver tissue TNF-α, IL-6, IL-1β, MDA, ROS, and Bax levels significantly increased, the liver tissue IL-10, SOD, GSH-Px, Bcl-2, p-MST1/MST1, p-LATS1/LATS1 and p-YAP/YAP proteins expression levels were significantly reduced (P<0.05). Compared with model group, the liver tissue injury was reduced in low-dose LID group, medium-dose LID group, and high-dose LID group, the cell apoptosis rate, serum AST, ALT, TBIL, LDH activity, liver tissue TNF-α, IL-6, IL-1β, MDA, ROS and Bax levels were significantly reduced, the liver tissue IL-10, SOD, GSH-Px, Bcl-2, p-MST1/MST1, p-LATS1/LATS1, and p-YAP/YAP proteins expression levels were significantly increased (P<0.05). Hippo-YAP signaling pathway inhibitor Verteporfin reversed the improvement effect of LID on ischemia-reperfusion injury in OLT rats (P<0.05). Conclusion: LID may activate the Hippo-YAP pathway, which reduce inflammatory response, oxidative stress, and liver cell apoptosis, and improve liver ischemia-reperfusion injury in OLT rats.
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Overview of the research of Q fever in animal models

li jinchun, yin jiaxiang

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Q fever is a zoonotic disease caused by Coxiella burnetii infection, which is widely spread in nature. Animal models are important tools to study the etiology and pathogenesis of infectious diseases and evaluate the effectiveness of vaccines. In recent years, a variety of animal models such as invertebrates, rodents and non-human primates have been used to study Q fever. This paper summarizes the research status of different Q fever animal models, discusses the advantages and disadvantages of these models, and summarizes the requirements and standards of future modeling work.
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Advances in the application of laser speckle contrast imaging in animal models of chronic cerebral hypoperfusion

Tangxin, tanjie

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Laser speckle contrast imaging technology can be used to dynamically measure microcirculation blood flow in tissues or organs in a visual and quantifiable way. Because of its advantages of in vivo detection, real-time imaging and simple operation, it has been applied in many fields of microcirculation detection.The animal model of chronic cerebral hypoperfusion is mainly constructed by reducing the bilateral common carotid artery blood flow to the brain, which can cause long-term insufficient cerebral blood supply. Laser speckle contrast imaging technology can observe and analyze the cortical cerebral blood flow, collateral circulation opening, neurovascular coupling response, etc., in the animal model of chronic cerebral hypoperfusion , so as to judge the success of animal model modeling and the therapeutic effect of intervention methods. In this paper, the application and advantages and disadvantages of laser speckle contrast imaging technology in the animal model of chronic cerebral hypoperfusion were summarized in order to provide new ideas for clinical treatment and scientific research.
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Research progress of berberine in the field of neuroprotection in ischemic stroke

lihongyu, lanrui

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Berberine is a natural Isoquinoline alkaloid, which can be initially used as a broad-spectrum antibacterial agent in clinical treatment of enteritis, peptic ulcer, chronic gastritis, pneumonia and other diseases. In recent years, with the in-depth study of the pharmacological effects of Berberine, more and more evidence shows that Berberine has neuroprotective effects on ischemic stroke. In this review, we introduced the intervention of Berberine on risk factors of ischemic stroke, and discussed the neuroprotective effects of Berberine in different mechanisms of ischemic stroke in detail, aiming to provide some reference for clinical and basic research in this field.
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Advances in Research on Mechanisms Related to Myocardial Regeneration in Neonatal Rats

chenmengqi

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Cardiovascular disease is a health hazard to humans and systolic heart failure due to myocardial infarction is a major cause of death. It was previously thought that myocardial cells of adult mammalian heart possess a limited ability to proliferate and renew themselves, and that after ischemic injury, a large number of myocardial cells are lost and eventually replaced by non-contractile scar tissue. In contrast, it has been widely reported that mammals have the ability to regenerate myocardium which is restricted to early postnatal life, and that it is strong enough to repair damaged heart tissue. The discovery of myocardial regeneration in neonatal heart has provided an ideal animal model to investigate the mechanisms that affect myocardial cell proliferation, and subsequently many mechanisms that can reverse myocardial cell cycle arrest and promote myocardial cell proliferation have been revealed. In this paper, we review the factors affecting myocardial regeneration gene expression (ncRNAs, transcription factors, etc.), myocardial regeneration-related signaling pathways, and the regulation of myocardial regeneration by non-myocardial cells (extracellular matrix, immune response, epicardium, etc.), so as to provide directions for achieving myocardial regeneration after myocardial injury in adult mammals.
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Establishment of genetic monitoring methods for experimental quail

heyang, zhangxiulin, zhangqiuyu, zhangxiaolu, fubo, wangwendong, duxiaoyan, chenzhenwen, lichanglong

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Objective To establish a genetic monitoring method for laboratory quails. Methods Quail microsatellite loci were screened through literature search, and microsatellite DNA loci suitable for quail were screened by interspecific transfer method in quail closely related species, chickens and ducks. Quail liver tissue DNA was extracted as a template, and the corresponding loci were screened by PCR amplification and agarose gel electrophoresis. Finally, based on the amplification of the selected microsatellite loci, the number of alleles, and polymorphism, microsatellite loci combinations for quail genetic quality detection were selected and detection methods were established. Results We preliminary determined 23 microsatellite loci for genetic monitoring of closed-colony laboratory quails. Conclusion A genetic monitoring method for laboratory quails is preliminary established.
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Innovation and exploration of Medical Laboratory Animal Science teaching based on smart teaching environment

YangZiHao

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Objective In the traditional laboratory zoology lecture environment, there is less teacher-student interaction, less student interest and less engagement in learning.In order to further improve the teaching quality of laboratory zoology, Methods this teaching and research department based on the different teaching environment of multimedia classroom and intelligent classroom, the theoretical course teaching of Medical Laboratory Zoology as the research ,object, the course lecture format, teaching mode, teaching methods and other aspects of innovation and exploration. The study used questionnaires to understand changes in student engagement in learning and preferences for smart classroom use, and NVivo qualitative analysis software to code student classroom behaviour. Results The smart teaching environment resulted in higher student interest and more frequent teacher-student interaction in the classroom. At the same time, students are significantly more engaged in learning than in traditional teaching, with higher correct rates on in-class and post-lesson exercises and a better grasp of concepts related to laboratory zoology. Conclusions In summary, the smart teaching environment can bring students a better feeling and experience, improve their interest in laboratory zoology, increase classroom learning engagement and achieve good teaching results.
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Progression of tripterygium wilfordii polyglycoside in mice with premature ovarian insuffici-ency model at different time points

马林纳, makun, fanxiaodi, luojie, lijiani, zhanghan

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Objective The changes of relevant indexes in the mice model of early-onset ovarian insufficiency caused by tripterygium wilfordii polyglycoside were discussed, and the best time point for intervention was determined. Methods Forty female ICR mice were randomly divided into blank group, A, B, C, and D model groups, with 8 mice in each group. The blank group was given gavage purified water for 14d (0.01ml/10g), and the remaining groups were given tripterygium wilfordii polyglycoside suspension (80mg/kg, 0.01ml/10g) for 1d (A model group), 3d (B model group), 7d (C model group), 14d (D model group), and the materials were taken in batches. Weigh the body weight, wet weight uterus and bilateral ovaries of mice in each group; Serum FSH, LH, E2, P, AMH, INH-B and T contents were detected by enzyme-linked immunoassay. HE staining observed the number and development status of follicles and corpus luteum at all levels of mice in each group. TUNEL fluorescence staining method detected the apoptosis area in the ovaries of mice in each group. The IHC method detected the positive expression of VEGFA, CD34 and EPO proteins in the ovaries of mice in each group. The mRNA expression of HIF-1α, SDF-1 and CXCR4 in each group of mice was detected by PCR. Results Compared with the blank group, the changes of indicators in model A did not meet the POI modeling standard. The ovarian index, uterine index and body weight of mice in the B model group decreased significantly (P<0.01), the weight of the C model group decreased significantly (P<0.01), and the ovarian index of the D model group decreased significantly (P<0.05). The serum indexes of the B, C and D model groups increased the contents of FSH and LH (P<0.01 or P<0.05), and the contents of E2, PROG, AMH, INH-B and T decreased (P<0.01). The number of basal follicles, presinus follicles, sinusoidal follicles, antral follicles, preovulatory follicles and corpus luteum decreased significantly (P<0.01 or P<0.05) and the number of atresia follicles increased significantly (P<0.01) in the B, C and D model groups. The apoptosis area of TUNEL fluorescent staining in A, B, C, and D model groups increased significantly (P<0.01 or P<0.05). The positive expression of CD34, VEGFA and EPO in the B, C and D model groups decreased significantly (P<0.01 or P<0.05). The expression of mRNA in the A and B model groups of HIF-1α, SDF-1 and CXCR4 was significantly increased (P<0.01 or P<0.05). Compared with the B model group, the relevant indexes of the C and D model groups changed significantly, indicating that the C and D models were more serious and tended to develop POF. Conclusion The B model group is the turning point of ovarian function from impaired POI to irreversible POF, suggesting that 3d administration of tripterygium wilfordii polyglycoside is the best time to induce POI disease model and effective drug intervention.
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Research progress of noncoding RNA in methamphetamine-induced addiction and neurotoxicity

zhang shu wei, cheng hao, wang hao wei, miao lin, li yi, guan li na, zeng xiao feng

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Methamphetamine (METH) is highly addictive and neurotoxic, which can cause cognitive and memory dysfunction in abusers. The harm of METH lies not only in its own toxicity, but also in the high physical and mental dependence of drug addicts, often causing mental disorders and causing violent behavior, bringing great safety risks to society. Non-coding RNA (ncRNA) does not code for proteins and is an important factor in regulating gene expression at the post-transcriptional level. Studies have shown that ncRNA plays an important regulatory role in methamphetamine-induced addiction and neurotoxicity, but the specific mechanism is unclear. This article reviews the current research progress of ncRNA in regulating METH-induced addiction and neurotoxicity, in order to provide a reference for ncRNA as a forensic identification index and potential drug intervention target for METH abusers.
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Advances in the mechanism of action of cyclic RNA in Parkinson's disease

liujuan, Li Yanjie, Qin hewei, Ma luyao, Zhao nannan, Xu zhenhua

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Parkinson's disease (PD) is a neurodegenerative disease characterized by the degenerative death of dopaminergic neurons in the substantia nigra, exhibiting a range of motor and non-motor symptoms that have a serious impact on the quality of life of patients. Circular RNA (circRNA, CircRNA) is a covalent closed-loop noncoding RNA that plays an important role in the progression of PD disease. This article reviews the involvement of circRNA in oxidative stress, regulation of transcriptional levels, neuroinflammation, autophagy, and α-synuclein.
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Analysis of application characteristics of acute liver injury animal model based on data mining

huyilong, zhangshuangli, qiuguangnan, fengyifan, miaomingsan, miaojinxin

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Objective To investigate the modeling elements of various types of animal models for acute liver injury, and to provide references and suggestions for the establishment and evaluation of animal models for ALI. Methods The animal experimental literature of acute liver injury from 2002 to 2022 was searched in the databases of China Knowledge Network, WanFang, Chongqing Vip, Chinese Medical Journal Full Text Data, PubMed, etc. The animal species, positive control drugs, modeling methods, modeling drugs and drug administration of the animal models of acute liver injury involved in the literature were summarized and summarized. The results were analyzed using Excel, SPSS Modeler18.0 and Cytoscape3.8.2. Results A total of 896 papers were included in the database. The most used animal models for acute liver injury were male KM mice; the modeling methods were mainly chemical liver injury, alcoholic liver injury, drug-related liver injury and immune liver injury, and the corresponding main modeling methods were : ① intraperitoneal injection of 10.0 mL 0.1% CCl4 vegetable oil, 24 h before the experiment; ② gavage of 12.0 mL 50.0%-56.0% ethanol, 16 h before the experiment; ③intraperitoneal injection of APAP 300 mg/kg, 24 h before the experiment; ④ tail vein injection of Con A 20 mg/kg, 8 h before the experiment. The evaluation of the model was based on liver pathological indexes as the gold index, combined with biochemical indexes Serum ALT, AST, liver tissue homogenate SOD, MDA content and activity were used as direct indicators. Conclusions Since the causes of acute liver injury vary in clinical practice, the preparation of animal models of acute liver injury should be based on the specific study content and characteristics of the study, and the corresponding modeling methods should be selected.
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The mechanism of Yantiao fang regulating Rho/ROCK signaling pathway on apoptosis of intestinal epithelial cells in mice with acute gastrointestinal injury caused by sepsis

Chen Qian, Wang D, Zhang DY, Jia SL, Wang LH, Cao YJ, Li YH

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Objective To investigate the effect of Yantiao Formula on apoptosis of intestinal epithelial cells in mice with acute gastrointestinal injury caused by sepsis by regulating Rho/ROCK signaling pathway. Methods 70 BALB/c mice were randomly divided into blank group (10 mice), sham operation group (10 mice) and model group (50 mice).Mice in blank group were fed normally without treatment.Sham operation group mice only open free cecum without perforation ligation;A mouse model of acute gastrointestinal injury caused by sepsis was established by cecal ligation and perforation (CLP). The mice were randomly divided into model group, Yantiao formula low-dose, medium-dose and high-dose groups, and ROCK inhibitor group.Hematoxylin-eosin (HE) staining was used to observe the histopathological changes of mice ileum.Serum levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) were determined by ELISA.The expression of PCNA and Ki-67 in mouse ileal cells was detected by immunohistochemistry.The expressions of Caspase 3 and Bax were detected by western blotting.The expression of ROCK mRNA and MLC mRNA in the Rho/ROCK pathway of mouse ileum were detected by RT-qPCR. Results The intestinal mucosa of the ileum tissue of mice with acute gastrointestinal injury caused by sepsis was atrophied obviously, villi were disordered, rupture and shedding were observed, epithelial cells were necrotic and shedding, inflammatory cell infiltration was obvious, and Chiu's pathological score was increased.Compared with blank group and sham group, the serum levels of pro-inflammatory mediators (IL-1β, IL-6, TNF-α) and mRNA levels of Caspase 3, Bax, ROCK and MLC in peripheral blood of mice in model group were increased, while the levels of anti-inflammatory mediators (IL-10) and expressions of PCNA and Ki-67 in ileum were decreased.Compared with model group, the histopathological changes of ileum in all Yantiao fang groups were improved to varying degrees with the increase of dose: the pathological score of Chiu's was decreased, the levels of IL-1β, IL-6 and TNF-α in serum were decreased, and the levels of IL-10 were increased.In addition, the expressions of PCNA and Ki-67 were increased, while the expressions of Caspase 3, Bax, ROCK mRNA and MLC mRNA were decreased. Conclusion Yantiao fang can inhibit the apoptosis of intestinal epithelial cells in mice with acute gastrointestinal injury caused by sepsis by regulating Rho/ROCK signaling pathway, so as to reduce the inflammatory reaction of intestinal tissue and ultimately prevent the damage of intestinal mucosal tissue.
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Research status and trend of animal models of depression: a bibliometric analysis based on CiteSpace

YANG JIAHUI, LIN MENG, LUO XIAOQUAN, LUO TAO, GONG MEIFU

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【Abstract】Objective With the help of literature metrology, the scientific literature in the field of animal models of depression was analyzed, so as to better understand the development trends and hot spots in this field.Methods We obtained publications on depression and animal models from 2013 to 2022 from the Web of Science core set (WOSCC) database. Citespace 6.1R 1(64-bit) Basic was used to analyze the annual publications, countries, institutions, authors and keywords related to this field.Results A total of 1000 articles were included in this study. From 2013 to 2022, the number of papers published gradually increased and stabilized. In terms of the number of articles, the United States has the most published articles (256) and the most Polish Academy of Sciences (50) . Wegener Gregers is considered the most influential author in the field, with 23 published articles. When analyzing keywords, “Animal Model” was the most frequent, followed by“Major depression”. Conclusions This study highlights the important research trends and hot spots in the field of animal models of depression. The US, China and Japan are leading the way in terms of publication, indicating their significant contribution to the development of animal models of depression. However, international cooperation is limited and there is more cooperation within institutions and groups. The field focuses on signaling pathways and therapeutic approaches to determine the pathogenesis of depression and better treatments. The study provides a visual analysis of trends in depression research to help researchers keep abreast of the latest developments.
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Effect of gender difference on the model of rheumatoid arthritis induced by bovine type II collagen

Sun Wenting, Wan Yingying, Yang Jiaxi, Wang Wenqian, Wang Haonan, Ye Wanting, Kou Qiuai

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Objective To construct female and male bovine collagen-induced arthritis (CIA) models and compare the effects of gender differences on the joint and extra-articular manifestations of CIA models. Methods The CIA model was induced by injection of bovine type II collagen and Freund's complete adjuvant into female and male SD rats. The general condition, arthritis index, foot swelling, serum inflammatory factors and plasminogen activator inhibitor levels, spleen index, knee and ankle joint pathology, right rear paw bone destruction, and pulmonary interstitial lesions of rats in each group were evaluated. Results The arthritis index of female CIA rats was significantly higher than that of male CIA rats on the 21st day after initial immunization (P<0.05), but there was no significant difference in the degree of foot swelling between the two groups at any time point of observation (P>0.05); Serum tumor necrosis factor α, interleukin1β and spleen index of female CIA rats were significantly higher than those of male CIA rats (P<0.001; P<0.001; P<0.05), there was no significant difference in plasminogen activator inhibitor levels (P>0.05); The scores of inflammatory cell infiltration and synovial hyperplasia in the knee and ankle pathology of female CIA rats were significantly higher than those of male CIA rats (P<0.05), and the cartilage damage of knee joint and the bone damage of right rear paw of female CIA rats were significantly higher than that of male rats (P<0.05); Both male and female CIA rats showed pulmonary interstitial inflammatory cell infiltration and mild fibrosis, but the pulmonary interstitial lesions in females were more severe than those in males. Conclusion Both female and male CIA models constructed with SD rats can have both arthritis and pulmonary interstitial lesions, but the lesion degree of female CIA rats is more serious. When using CIA models for RA related research, attention should be paid to the impact of gender differences.
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Effects and mechanism of NCTD on proliferation and apoptosis of human leukemia cells by targeting PPP5C

zhangxin, cuibingjie, yuguoxing, wangfei, zhaoliang, gaona, dujing

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Objective To study the effects and mechanism of norcantharidin (NCTD) on proliferation and apoptosis of human leukemia NB4 and K562 cells by targeting phosphoprotein phosphatase 5 catalytic (PPP5C). Methods NB4 and K562 cells were cultured in vitro, and the pcDNA3.1 and PPP5C-pcDNA3.1 plasmids were electroporated into NB4 and K562 cells. NB4 and K562 stable cell lines were screened with geneticin (G418). The protein and mRNA expression levels of PPP5C were identified by Western blot and qRT-PCR. The proliferation ability, migration ability and apoptosis rate of NB4、K562 cells were determined by CCK-8 assay, transwell assay and the Live DeadTM animal cell viability/toxicity detection kit. NB4 and K562 cells were divided into control group and different doses of NCTD group, and cultured in 1640 medium containing 0, 8, 16, 32 μg/ml NCTD. The Live DeadTM animal cell viability/toxicity detection kit detected the number of dead and live cells and cell morphology was recorded by microscope. Western blot was used to detect the protein expression levels of caspase 3, Cleaved caspase 3, JNK, p-JNK, p38, p-p38 and α-tubulin in cells of each group. Results? the proliferation ability of cells, the migration ability and apoptosis rate of NB4、K562 cells are enhanced after overexpression of PPP5C in human leukemia NB4 and K562 cells; Compared with the control group, each concentration group of NCTD promoted apoptosis in a dose-dependent manner; PPP5C overexpression antagonizes the killing effect of NCTD on leukemia cells. Conclusions NCTD can promote the apoptosis of NB4 and K562 cells and inhibit the proliferation of cells by inhibiting PPP5C.
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Research on the Mechanism of LSC Immune Escape with Intervention by TCM

ZHANG Meiling, 章, CuiYaru, ChengShupeng, LingZhiming

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Leukaemia is a critical disease with a high incidence in clinic at present, with an extremely high fatality rate. Among them, immune escape from leukaemia stemcells(LSC) is the main factor for recurrence and progression after leukaemia-induced remission. The clinical diagnosis and treatment of TCM has distinct advantages of syndrome differentiation and treatment. Based on the purpose of diagnosis and treatment, the treatment of leukaemia by TCM emphasises the "harmony of yin and yang" to estore human function, which is conducive to improving the body's autoimmunity and conforms to the mechanism of intervention for tumour cell immunity escape. This article discusses the echanism and research progress of TCM intervention in Lsc immune escape from literature research and TCM theory.
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Effects of polysaccharide content and anti-inflammatory, hemostatic and antioxidant activity before and after preparation of Mosla chinensis-jiangxiangru

Maqiuting, Xulei, Zhuyuchen, Xumengting, Zhangwenkai, Liuzhiyong

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Abstract：Objective:Exploring the changes in polysaccharides in Jiangxiangyu before and after giner juice, and evaluation of polysaccharide anti -inflammatory and antioxidant antioxidant activity before and after the processing. Methods: The content of polysaccharides beforeand after processing was determined by phenol-sulfuric acid method（Elsholtzia chinensis polysaccharide-JXRPs, Ginger Elsholtzia chinensis polysaccharide-JZJXRPs); The body internal uses the swelling model of rats and the body fat polysaccharide (LPS) to induce mousemacrophages RAW264.7 inflammation model.The best administration concentration is selected by using cell proliferation (MTT) method, Elisa method measures the expression of IL-6, IL-12, NO, IL-4, and IL-10 in the cells;Observe the bleeding time of mice to evaluate its hemostatic effect by observing the tail -cutting method; finally, use the ability to remove DPPH and ABTS to evaluate its in vitro antioxidant activity.Results: The contents of JXRPs and JZJXRPs were 13% and 22%,As a result of the swelling of rats, after 4h in injection, compared with the model group, JXRPs ppear significant difference in dosage doses of 200 mg/kg (P <0.05), and JZJXRPs When the dose is 100 mg/kg, you can significantly reduce the swelling of rats (P <0.05);The in vitro anti-inflammatory results show that the polysaccharides before and after the processing can significantly inhibit cell secretion of IL-6, IL-12 and NO (P <0.01), promote cell secretion of IL-4 and IL-10 (P <0.01), and the processing of the processing The post -effects are stronger.The results of the mouse break the hemostatic experiment show that: compared with the control group, the JXRPs group can speed up the hemostatic effect but there is no significant difference, and there is asignificant difference in the dosage of the JZJXRPs (P <0.05) in the medium dose (P <0.05), and the High doses have accelerated trend but there is no significant difference; The results of antioxidant activity in vitro showed that JXRPs and JZJXRPs had different degrees of scavenging ability for DPPH and ABTS, with IC50 values of JXRPs of 0.2215 mg/ml and 0.2110 mg/ml of JZXRPs, respectively, and IC50 values of 0.1651 mg/ml and 0.1884 mg/ml of JZJXRPs, respectively.Conclusion:After the Jiangxiangyu is produced by ginger juice, it can promote the dissolution of polysaccharides and increase the polysaccharide content. JZJXRPS anti -inflammatory hemostasis and antioxidant capacity are stronger than JXRPS, which can lay the foundation for the follow -up research and clinical application of JXRPS.
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Research progress of SHP-2 in tumor-associated macrophages

wuxueliang

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Abstract: Tumor-associated macrophages (TAMs) are the dominant cell group in the tumor microenvironment (TME) and are the most important regulatory cells of immune system suppression and tumor cell proliferation in Tmes. Src homologous 2 protein tyrosine phosphatase 2 (SHP-2) is a non-receptor protein tyrosine phosphatase that plays an important role in signaling from the cell surface to the nucleus and is a key intracellular regulatory factor mediating cell proliferation and differentiation, involved in a variety of growth factor and cytokine signaling pathways. Recent studies have shown that SHP-2 is a key enzyme that determines the function of tumor-associated macrophages, but because of its variable function, it plays different or even opposite roles in different solid tumor microenvironments. Based on this, this paper reviews the function of SHP-2 in TAMs and the role of ShP-2 in related solid tumors, providing a solid scientific basis for tumor immunity and targeted therapy.
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Antitumor mechanism of Ardisia Crenata

renqunli

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Ardisia Crenata Radix is a traditional Chinese medicine, which belongs to Myrsinaceae, and its main components are coumarins, saponins, flavonoids and volatile oil. Bergenin, ardisicrenoside A, ardisicrenoside B,ardisiacripin A,ardisiacripin B and embelin are active anticancer compounds with the in-depth study of the anti-tumor effect of Ardisia Crenata Radix. They show high potential in oral cancer, nasopharyngeal carcinoma, liver cancer, colon cancer, bladder cancer, cervical cancer and leukemia mainly through inducing tumor cell apoptosis, increasing tumor cytotoxicity, inhibiting cell proliferation, inhibiting tumor cell metastasis and migration, and inducing cell regulatory enzyme cascade reaction. However, the preclinical experimental data of cinnabar root anti-tumor mechanism are lack of high-quality, multi-sample and multi-repeated randomized controlled trials, and the clinical research data are lack of tumor prognosis, pharmacodynamics and pharmacokinetic data. Accurate research experiments and clinical trials should be designed to further explore the pharmacological effects of mining cinnabar root.
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Research progress in immunoregulation mechanism of exosomes on bacterial infection

李, Lizhiwei

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Exosomes are small endosomal derived extracellular vesicles with lipid bilayer structure, which contain substances such as protein, lipids, DNA, RNA, miRNA and lncRNA. Exosomes participate in pathogen recognition, antigen presentation, autophagy regulation, immune activation and immunosuppression in bacterial infection. Studies have shown that miRNA, lncRNA and protein in exosomes play important roles in regulating antibacterial reaction of organism. We reviewed the immunomodulatory effects of exosomes on several intracellular and extracellular bacterial infections to provide evidence for studying the interaction between exosomes and bacterial infections.
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Application and challenges for NHP laboratory animals in neuroscience

HuLingfeng, FanShengtao, LiuJie

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【Abstract】: Currently, non-human primates (NHPs) are becoming increasingly important in laboratory animals, especially in the field of neuroscience, where many significant breakthroughs have been made, including research on brain development, neurodegenerative diseases and psychiatric disorders, but as their breeding and use grows, biosafety and animal ethics issues should be taken into account. This review summarizes the application and challenges of NHP laboratory animal in the neuroscience field from the aspects of NHP overview, feeding and operation, biosafety, and animal ethics.
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Research progress on evaluation of type 2 diabetic peripheral neuropathy animal model

zhuziyue

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Diabetic peripheral neuropathy is a common diabetic complication. At the moment, our understanding of its pathogenesis is incomplete, and there are no effective treatment options. In-depth research requires the use of animal experiments. The criteria for modeling success and the evaluation method for peripheral nerve function recovery are critical for carrying out animal experiments on type 2 diabetic peripheral neuropathy, but there is a lack of sorting out and analyzing the evaluation methods for type 2 diabetic peripheral neuropathy models. As a result, the author reviewed recent data, summarized and analyzed the evaluation methods of animal models of type 2 diabetic peripheral neuropathy from small and large nerve fibers, and proposed future development directions in order to provide a reference for related research.
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A review and promising future directions of machine learning in laboratory animal facility management

xuxiao, Chen Qi

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As the intelligence level gradual improving in domestic laboratory animal facilities，a large amount of valuable data has been accumulated. The data has not been fully exploited due to lacking of analytical means. In the context of Big data, Machine learning algorithms have achieved remarkable results in biomedical, building science and other fields, and also provide a reference for their application in laboratory animal facility management. In this paper, the contents, methods and models of machine learning methods applied to various systems of laboratory animal facilities at home and abroad are reviewed and prospected.
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Optimization of the preparation method of lung tissue cryosections for multiplex immunofluorescence staining

Ye Qianchen, Xu Dan, Wen Fuqiang, Chen Jun, WANG TAO

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Objective Optimizing the preparation method of mouse lung cryosections to improve the quality of lung cryosections helps to enhance the specificity of immunofluorescence staining and obtain more accurate and reliable experimental results. Methods C57BL/6 mice were used to make cryosections by the traditional post-freezing fixation method, the pre-freezing fixation method, and a modified perfusion pre-freezing fixation method, respectively. A laser scanning confocal fluorescence microscope was used to observe lung tissue immunofluorescence staining. The whole areas of mouse lung slices were scanned by fluorescence microscope, and then the numbers of intact airways per unit area of lung tissue were calculated. Results For the lung cryosections made by the traditional post-freezing fixation method, the alveoli structure was damaged, and the airway wall was seriously broken with non-specific staining. The lung cryosections made by the pre-freezing fixation method showed relatively intact alveolar and airway structures but collapsed alveoli and several destroyed airways. The structure and morphology of the alveoli and airways were intact and clear in the lung cryosections prepared by the modified perfusion pre-freezing fixation method. In addition, the locations of target genes were accurate with multiple immunofluorescence staining. The number of intact airways (diameter ≥100 μm) per unit area in the lung cryosections from the modified perfusion pre-freezing fixation method was higher than from the pre-freezing fixation method (0.66±0.15 /mm2 vs. 0.33±0.14 /mm2, P<0.05), and was also significantly higher than that from the traditional post-freezing fixation method (0.66±0.15 /mm2 vs. 0.02±0.04 /mm2, P<0.01). Conclusions The modified perfusion pre-freezing fixation method is beneficial to maintain mouse lung tissue's morphological integrity and obtain high-quality multiplex immunofluorescence staining results.
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To explore the effects of different types of drinking water on the growth and fecal flora of mice

wuxuying

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【Abstract】 Objective to explore the effects of different types of drinking water on growth and fecal flora of mice. Methods SPF NIH mice were selected and divided into 5 groups with 32 males and females in each group. they were fed with pure water (control group), acidified water, alkalized water, weak acid water and solid water, respectively. diet and body weight were monitored continuously for 20 days. after the experiment, animal feces samples were collected, and the V3-V4 region was amplified with bacterial16S rDNA universal primers. Illumina Miseq high-throughput sequencing platform was used for high-throughput sequencing, and microbial community, alpha diversity and beta diversity were analyzed by bioinformatics method. Results in terms of body weight, the water of weak acid in female mice was higher than that in the control group at different pH values, while the other groups were lower than that in the control group(P﹥0.05). in male mice, the body weight of acidified water group was higher than that of control group, while that of other groups was lower than that of control group, but there was no statistical difference between groups(P﹥0.05). the body weight of female and male mice with solid water was lower than that of control group(P < 0.05). in terms of food intake and water intake, the water intake and water intake of female mice in the alkalized water group were lower than that of other groups, and the water intake of female and male mice in the solid water group was lower than that of other groups. through OTU cluster analysis, the dilution curve showed that the data volume of this sequencing was reasonable. the fecal flora of NIH mice was divided into five phyla, among which bacteroidetes and firmicutes were the main phyla. at the genus level, pseudopurpuromonas, lactobacillus and mycobacterium were the main genera. there were differences in fecal flora abundance and diversity among the five drinking water types. alpha analysis showed that the acidified water group had the highest flora abundance and diversity, while the solid water group had the lowest flora diversity. beta analysis showed that the fecal flora of the solid water group and the control group were the most similar, followed by alkalized water group, acidified water group and weak acid water group, respectively. Conclusions through the exploration of different types of drinking water, it is revealed that the solid form of drinking water has a great effect on the body weight, feed intake, water intake and fecal flora of mice, and the abundance and diversity of fecal flora of mice are affected by different pH values of drinking water, especially acidified water has a greater effect on the fecal flora of mice.
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The therapeutic effect of licorice zinc on chloasma mice was explored based on nrF-2 /HO-1 pathway

Du Xiaoshuang, Liu Ping, Deng Ying, Yang Hongqiu, Du Yu

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[Abstract] Objective To investigate the therapeutic effect of licorice zinc on melasma. Methods Melasma was induced by 100 mJ/cm2 UVB irradiation combined with 15 mg/kg progesterone injection. Tranexamic acid (0.065 g/kg) and low (0.65 g/kg)/medium (1.3 g/kg)/high (2.6 g/kg) zinc licorice were treated for 14 days. Skin was taken for HE and Masson-Fontana staining; and SOD, MDA, GSP-Px, TNF-α, IL-1β and IL-6 contents; plasma protein Nrf-2, nuclear protein Nrf-2, and HO-1 expression levels were measured. Results High dose of zinc licorice significantly reduced melanocyte formation, collagen cell necrosis and inflammatory infiltration, significantly up-regulated the expression of GSP-Px and SOD, decreased the expression of MDA, IL-6, IL-1β and TNF-α, up-regulated the expression of nuclear proteins Nrf-2 and HO-1, and down-regulated the expression of plasma protein Nrf-2. Conclusion Zinc licorice activates Nrf-2/HO-1 pathway to initiate high expression of HO-1, SOD and GSP-Px against oxidative stress, thereby reducing melanogenesis.
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Study on the mechanism of oral microflora involved in areca nut extract induced oral ulcer in rats

pengdongdong, chenxiangchi, tangzining, liuxuewu, yuanxiangzhong, limeng, liqiao, zhangzeheng

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Objective The model of oral ulcer in rats was constructed by areca nuts extract, and the structural changes and diversity characteristics of oral flora were observed, so as to explore the pathogenesis of oral flora involved in oral ulcer in rats induced by areca nuts extract, providing theoretical support for clinical prevention and treatment of oral ulcer. Methods Thirty SD rats were randomly divided into normal group, model group, drug treatment group, 10 rats/group. The rat oral mucosa was injected with 10g/mL areca nuts extract subcutaneously to replicate the rat oral ulcer model. Ulceration area, ulceration score, and levels of TNF-α, IL-2, and IL-8 in local tissues were observed, and HE staining was performed on oral mucosal tissues to observe the morphological changes of oral mucosal tissues. High-throughput sequencing method was used to analyze the structure distribution of oral microbial flora and microbial community diversity. Results Compared with normal group, the ulcer area of rats in model group was significantly increased (P<0.01), the ulcer score was significantly increased (P<0.01), the levels of IL-2, IL-8 and TNF-α in oral mucosal tissue were significantly increased (P<0.01), and the shannon index of oral saliva of rats was significantly increased (P<0.05).simpson index was significantly decreased (P<0.01), Strep-tococcus and Veillonella were significantly decreased (P<0.05,0.01), oral mucosal epithelial cell proliferation or focal necrosis, mucosal lamina propria edema and hemorrhage were observed in model group. It was accompanied by abundant infiltration of neutrophils and monocytes. Compared with model group, the ulcer area and ulcer score of model group were significantly decreased (P<0.05), the levels of IL-2, IL-8 and TNF-α in oral mucosal tissue were significantly decreased (P<0.05,0.01), and the shannon index of oral saliva of rats was significantly decreased (P<0.05). Simpson index was significantly increased (P<0.01), Strep-tococcus was significantly increased (P<0.001), Staphylococcus was significantly decreased (P<0.01), and the pathological degree of oral mucosa was significantly improved. Conclusion Areca nuts extract can successfully reproduce the rat model of oral ulcer, and it is speculated that the development of oral ulcer disease induced by areca nuts extract may be related to the imbalance of oral flora and local tissue inflammatory mediators.
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Effects of 5-Aza-CdR on hippocampal neurogenesis in mice via the Notch1 pathway

wangbaojie, suliqing, yanlei, zhangzhiyong, 王志广, baosuya, shaoguo

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【 Abstract】 Objective To investigate the effect of 5-Aza-CdR on Notch1 pathway and neural regeneration, and to explore the effects of 5-Aza-CdR on learning memory ability in mice by exploring active avoidance behavioral experiments on mice. Methods Sixty 6- to 8-week-old ICR male SPF-grade mice were divided into two groups, and 5-Aza-CdR was administered to one group of mice via lateral ventricular injection (i.c.v.), while the other group was injected with BSA as a control group. 5-Aza-CdR was administered to mice by lateral ventricular injection (i.c.v). mRNA and protein expression levels of Notch1 and HES1 were detected by real-time PCR and Western blot 24 hours after injection; 5-bromo-2'-deoxyuridine (BrdU)-positive cells were observed by laser confocal microscopy and Notch1 expression in hippocampal DG by laser confocal microscopy; Notch1 methylation changes were detected by MS-PCR; and learning and memory behaviours of mice were assessed by measuring passive avoidance tests and shuttle avoidance assays. RESULTS Injection of 5-Aza-CdR increased hippocampal Notch1 pathway activity and promoted neuronal regeneration in the DG region, decreased methylation levels in the Notch1 promoter region, and enhanced the ability of mice to perform active avoidance behaviour. Conclusion The effect of 5-Aza-CdR on active avoidance behavior may be related to the influence of hippocampal neural regeneration through the Notch1 pathway.
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Effects of emodin on autophagy and cycle arrest in fibroblast-like synoviocytes in rheumatoid arthritis

Tao Bonan, WANG Yonglan, HONG Lan, YUAN Lin

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Objective: Based on the cGAS/STING signaling pathway to investigate the potential effect of emodin (EMD) on autophagy of human rheumatoid arthritis fibroblast synovial cells (MH7A). Methods: CCK-8 method was used to detect the results of MH7A cell proliferation, and the concentration of drug was screened according to cell survival rate. Then, autophagy inhibitor 3-MA was added to further verify the effect of emodin on autophagy. Autophagy of MH7A cells was detected by MDC method. The protein expression levels of cGAS, STING, p-STING, LC3-I, LC3-II, p62 and Beclin-1 were detected by Western blot. Results: MDC staining indicated that emodin could enhance autophagy of MH7A cells. Western Blot results indicated that emodin could decrease the expressions of autophagy related proteins cGAS, STING, p-STING and P62, and increase the expressions of LC3-II and Beclin-1 in MH7A cells. After addition of autophagy inhibitor 3-MA, the expression of P62 protein in MH7A cells increased, while the expression of LC3-II and Beclin-1 protein decreased. Conclusion: Emodin may accelerate autophagy and inhibit MH7A cell proliferation by down-regulating cGAS/STING signaling pathway.
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Progression of the Relationship between Pyrozosis and Atherosclerosis

huangshuning

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Pyroptosis is a programmed mode of death, and activated aspartase-1 (caspase-1) can induce the occurrence of pyroptosis, promoting the release of inflammatory factors. In recent years, studies have found that pyroptosis may be closely related to the occurrence, development and outcome of atherosclerosis. This article reviews the relevant studies of endothelial cells pyroptosis, vascular smooth muscle cells pyroptosis and macrophages pyroptosis in the development of atherosclerosis, aiming to provide new ideas for the pathogenesis and diagnosis and treatment of atherosclerosis.
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Gli2 regulates the activation of Hedgehog pathway on proliferation, metastasis and epithelial mesenchymal transformation of Tca8113 cells

Liu Maolin, Wang Xiaotang, Song Xiaona, Ma Yunfei, Chang Xiaoqi, Song Guohua

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Objective: To investigate the effects of Gli2 on the proliferation, growth, migration and invasion of oral cancer cells (Tca8113) at the cellular level, and to clarify the molecular mechanism of Gli2 regulation on the migration and invasion of oral cancer cells. Methods: siRNA was used to inhibit Gli2 expression in Tca8113 cells. The effects of Gli2 on the proliferation, growth, migration and invasion of Tca8113 cells were examined by CCK-8, plate cloning and transwell chamber assay. Further, qRT-PCR and Western blot were used to explore the mechanism of Gli2 regulation of malignant proliferation and metastasis of Tca8113 cells. Results: The mRNA and protein expression of Gli2 in oral cancer cells (Tca8113) were increased. Interference with Gli2 expression inhibited the proliferation, growth, migration and invasion of Tca8113 cells. Further studies showed that interfering with Gli2 expression inhibited mRNA and protein expression of key factors in Hedgehog (Hh) pathway. In addition, interference with Gli2 expression can significantly affect mRNA and protein expression of key factors in Epithelial mesenchymal transformation (EMT) pathway. Conclusion: Gli2 is abnormally activated during oral cancer, and interference with Gli2 expression significantly inhibits the proliferation, growth, migration and invasion of oral cancer cells. Gli2 influences the migration and invasion of oral cancer cells by regulating Hh pathway and EMT pathway. This study provides a new way to elucidate the pathogenesis of oral cancer and a new perspective for clinical treatment of oral cancer.
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A model study of blood in urine (bladder cancer) under scorching humid fever under MNU-induced SD rats

changtuo, wangjie, linan, wangtianqi

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Objective: To investigate the modeling process and mold formation rate of N-methyl-N-nitrosourea (MNU)-induced lower jiao dampness-heat syndrome uremia bladder cancer (BC) model. Methods: Batch samples were collected by bladder perfusion (MNU) and H&E staining and pathological observation of pathological tissues were carried out at a total of 6 time points before, during and after molding, so as to understand the formation and development of carcinoma in situ of the bladder. Results: The experimental process was smooth, and no obvious urinary tract bleeding in rats occurred during the operation. By this modeling technique, considerable bladder tumors can be obtained after the eighth week, and there are obvious epithelial hyperplasia, damage and large-scale tumor formation in the bladder of rats in the model group. Conclusion: MNU can induce SD rat bladder cancer model with obvious model formation and low mortality, and the experimental data can provide a certain reference for the establishment, improvement and application of bladder cancer model.
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Protective effects of HIF-1α pathway in cold storage of isolated organs

wangzhiyang, zhengsiyang, zhuliang

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Organ transplantation is the main treatment for organ failure. The functional protection of donor organs during ex vivo transportation is the key to the success of organ transplantation. How to protect the functions of donor organs during in vitro transportation is one of the key issues in the field of organ transplantation research. In a hypoxic environment, the transcriptional activity of a series of genes in cells is activated. These genes are mainly involved in angiogenesis, iron metabolism, glucose metabolism, and cell proliferation/survival. In aerobic organisms, hypoxia-inducible factor-1α (HIF-1α) is involved in the regulation of the expression of various genes to maintain the homeostasis of tissues and cells under hypoxic conditions, thereby adapting to the hypoxia. Many studies have shown that the HIF-1α pathway plays an important role in protecting isolated organs from cold ischemia injury during cold storage. HIF-1α has been a hot spot in the research on the protective mechanism of cold ischemia injury of isolated organs. The intervention of the HIF-1α-related signal pathway is expected to become a new strategy for maintaining organ function during cold storage of isolated organs.
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Advances in animal models of diet-induced nonalcoholic fatty liver disease

Wang Jialin, Wang Chongyang, Li Yang, Chen Xianwei, Yuan Zhongnan, Zou Chaoxia, Zou Chendan

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The establishment of scientific and effective animal models is a key step to complete disease research. Diet induction is a common method to establish animal models of nonalcoholic fatty liver disease (NAFLD). The common animal models of diet-induced NAFLD mainly include high-fat and high-sugar diet-induced model, high-fat and high-cholesterol diet-induced model, and choline-deficient diet-induced model. Due to the different nutrients ingested by different modeling methods, the pathological characteristics such as fatty deformation, inflammation and fibrosis of the liver are different. In addition, different animal models vary in disease progression, disease severity, and applicable studies. This article analyzes and compares the common animal models of NAFLD induced by different diets in modeling methods, modeling time, pathological characteristics, applicable research, and related advantages and disadvantages, so as to provide reference for NAFLD researchers to select animal models.
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Isolation and extraction of Kupffer cells and hepatic stellate cells in mouse liver

mawenmeng, wuhao, yanyutong, sunxun, zhengqianqian

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【】Objective It is to explore the extraction and purification methods of Kupffer cells and hepatic stellate cells from mouse liver, and provide reference and suggestions for the separation and extraction methodology of primary non parenchymal cells from mouse liver.Methods Based on in vivo collagenase perfusion digestion, different reagents and methods such as Percoll and OptiPrep were used to extract C57BL/6 mice Kupffer cells and hepatic stellate cells and evaluate the purity through flow cytometry and immunofluorescence methods. Results The two-layer Percoll method for extracting Kupffer cells and the two-layer OptiPrep method for extracting hepatic stellate cells are feasible,and the purity can reach more than 90%.The cell yield was 1~2×107/liver, the cell survival rate was more than 90%.After 48 hours of primary cell culture, the number of Kupffer cells F4/80-positive cells and hepatic stellate cells α-SMA-positive cells reached more than 75%. Conclusions The separation and extraction method of Kupffer cells and hepatic stellate cells from mouse liver is perfect, reliable, cost-effective and reproducible.
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Application Research Progress of Single-cell RNA-sequencing Technology in Neurodegenerative Diseases

Wujianfei, Wangbinglong

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Neurodegenerative diseases (NDs) are the mental diseases closely related to the central nervous system, characterized by morphological abnormalities and slowly progressive loss of function in specific neuron groups. The main diseases include Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic lateral sclerosis (ALS), Multiple sclerosis (MS) and Huntington's disease (HD). However, the directly therapies for NDs are not founded. In recent years, single-cell RNA-sequencing (scRNA-seq) technology has been widely used in various neurodegenerative diseases. It has been found that the pathogenesis of NDs are involved in conditions of immune cells and biological processes such as mitochondrial function, angiogenesis, inflammation and synaptic transmission. The antilepsis of induced pluripotent stem cells (iPSC) is a potential treatment for NDs. Ultimately, the application of scRNA-seq technology in various NDs was reviewed in this paper ,and provided reference for the future prevention and treatment of NDs.
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Research progress on modeling methods and evaluation indexes of kidney injury in zebrafish

lanailin, Huangchunhua, Xiaming, Limaojuan, Wangsiqi, Loudidong

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Renal function is to filter blood , regulate fluid and electrolyte balance, which is crucial for health of the body, moreover, the kidney is susceptible to toxicity of various compounds in and out of the body, resulting in renal function damage, hence the prevention and treatment of renal function injury caused by various factors is also a hot research topic. Zebrafish is an ideal animal model as it is closely related to humans in terms of morphology, physiology and function of kidney and its response to compounds. In this paper, we will review the methods and evaluation indexes of zebrafish kidney injury modeling.
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Microvascular morphometric analysis of cerebral cortical functional areas in C57BL/6 mice of different months of age

guomin

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Abstract: Objective To observe and analyze the different functional areas of cerebral cortex in C57BL/6 mice of different months. Methods Improved alkaline phosphatase staining was used to reveal the microvascular morphology of the cerebral cortex of C57BL/6 mice, including motor cortex (primary motor cortex, secondary motor cortex), sensory cortex (primary somatosensory cortex, secondary somatosensory cortex), visual cortex (primary visual cortex, secondary visual cortex), auditory cortex (primary auditory cortex, secondary auditory cortex), olfactory cortex (extrorhinal cortex, entorhinal cortex). Images were captured by OLMPUS BX51 microscope combined with Image-Pro Plus 5.1 software. The microvascular length density (Lv), microvascular surface area density (Sv) and microvascular volume density (Vv) were analyzed by Image-Pro Plus 5.1 software. Results The levels of alkaline phosphatase in microvessels of different functional areas of cerebral cortex increased with age and reached the peak in adults. There were four patterns for pia vessels to enter the cortex including T shape, Y shape, large arc, small arc. The Lv, Sv and Vv in different functional areas of the same aged mice showed a downtrend trend in the motor cortex, sensory cortex, visual cortex, auditory cortex and olfactory cortex. Moreover, the microvascular density of Lv, Sv and Vv in the motor cortex and sensory cortex was statistically significant compared with those in the olfactory cortex (P<0.05). The vascular densities of different functional areas in the aged mice were lower than those in the adult ones, but there was no statistical significance (P>0.05). Conclusion The improved alkaline phosphatase staining may clearly reveal the microvascular architecture in cerebral cortex of C57BL/6 mice and it provides morphological reference for the research of cerebrovascular diseases and the preparation of animal models.
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Research progress of traditional Chinese medicine for stroke based on epigenetic regulation

Fu Xue Qin

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Epigenetics is a branch of molecular biology, and is a research hotspot in the post-gene era in the field of life sciences. The application of epigenetic modification research methods is the frontier field of the pathogenesis of ischemic stroke, and it is the interpretation of traditional Chinese medicine in the treatment of ischemia. Targets of stroke and effective approaches to their mechanisms of action. At present, the etiology and pathogenesis of ischemic stroke has not been fully clarified, and modern medical treatment is still insufficient. The treatment of ischemic stroke with traditional Chinese medicine has unique advantages and broad prospects. The latest research has found that traditional Chinese medicine can participate in the regulation of abnormal epigenetic modification in the treatment of stroke. This article mainly starts from the epigenetic basis of traditional Chinese medicine theory of stroke and the application of DNA methylation, non-coding RNA and histone modification in stroke treatment and traditional Chinese medicine research, and explains the appearance of traditional Chinese medicine in the treatment of stroke. The role of heredity in order to provide new ideas and scientific basis for traditional Chinese medicine treatment of the disease
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Geniposide promotes skin ulcer wound healing in diabetic rats through PI3K/Akt pathway

chenxiaoyan

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Objective To investigate the protective effect of geniposide on diabetic skin ulcer and its mechanism. Methods Rats were divided into normal group, model group and geniposide subgroup (Gen-L: 200 mg/kg; Gen-H: 500 mg/kg). The diabetic rats were given normal saline or geniposide by intragastric administration (n = 6). Treatment was administered once a day, and the wound healing and inflammation of each group were recorded every day. After 7 days of treatment for diabetic skin ulcers, the wound area, tissue sections, TUNEL staining and Western blot were used to quantitatively analyze the changes of wound healing, apoptosis and related regulatory protein expression. Results Compared with the model group, geniposide (200 mg/kg and 500 mg/kg) orally could significantly promote the wound healing and increase the contraction of the injured area in diabetic rats. In the study of skin wound apoptosis in diabetic rats, TUNEL staining positive cells in geniposide subgroup were significantly reduced (P<0.05). Geniposide can significantly inhibit skin inflammation and promote wound repair, which may be related to the promotion of PI3K and Akt phosphorylation. Conclusion Geniposide can promote skin wound repair in diabetic rats by inhibiting inflammatory response and apoptosis.
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Effect of Dingkun Pill on PI3K/AKT/mTOR signal pathway in rats with endometriosis

wuxueliang

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[Abstract] Objective: To explore the effect of Dingkun Pill on PI3K/Akt/mTOR signaling pathway in rats with endometriosis (EMs). Methods: The EMs rat model was constructed by heterotopic transplantation of endometrial tissue and randomly divided into five groups: model group (M group), Dingkun Pill low (1.13g/kg) dose group (DKP-L group), Dingkun Pill medium (2.26g/kg) dose group (DKP-M group), Dingkun Pill high (4.52g/ kg) dose group (DKP-H group), gestrinone (60mg/kg) group (GES group), with 12 rats in each group. Another 12 normal SD rats were opened the abdomen without transplantation ectopic endometrial tissue, and set as sham operation group (sham group). The rats were killed after intervention with drugs, the volume of ectopic endometrium and the weight of ectopic lesions of rats in each group were measured, the microvessel density (CD31 positive rate) and the expression of VEGF and MMP-9 in rat ectopic endometrial tissue were detected by immunohistochemical staining; the rat serum VEGF, MMP-9, iNOS and TNF-α levels were detected by enzyme-linked immunosorbent assay (ELISA); the expression of PI3K/Akt/mTOR pathway related proteins in rat ectopic endometrial tissue was detected by western blotting. Results: Compared with the sham group, the microvessel density, VEGF and MMP-9 expression, serum VEGF, MMP-9, iNOS and TNF-α levels, p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR in the ectopic endometrial tissue were significantly increased in the M group (P<0.05); compared with the M group, the ectopic endometrial volume, the weight of the ectopic lesion, the microvessel density of the ectopic endometrial tissue, VEGF and MMP-9 expression, the serum VEGF, MMP-9, iNOS and TNF- α levels, p-PI3K/PI3K, p-Akt/Akt, p-mTOR/mTOR in ectopic endometrial tissue were all decreased in the drug intervention group, and DKP-L, DKP-M and DKP-H groups were dose-dependent (P<0.05); compared with the DKP-H group and the GES group, there was no significant difference in the indicators of rats (P>0.05). Conclusion: Dingkun Dan can reduce inflammation and inhibit ectopic endometrial growth in EMs rats, which may be achieved by blocking PI3K/Akt/mTOR signal pathway.
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Experimental Study on Mongolian Drugs Hatagaqi-7 Promoting Ulcer Wound Healing of diabetes Rats via HIF-1α

DongChenghai, Cheliger, ChaoRiya, manzhu, Bao Yonglin, GongLimin

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Objective: To study the effect of mongolian drugs Hatagaqi-7 promoting ulcer wound healing of diabetes rats via hypoxia inducible factor-1α(HIF-1α). Methods: Adult male SD rats were randomly divided into control group, diabetes group, mongolian drug group and cytokine group. Besides the control group, the other three groups were treated with intraperitoneal injection of streptozotocin to establish the diabetes model. The ulcer wounds were prepared in the back of the four groups. One week later, the mongolian drug group was treated with hattagelge-7, and the cytokine group was treated with recombinant bovine basic fibroblast growth factor for two consecutive weeks. Then fasting blood glucose (FBG), wound area, wound pathology, the expression level of advanced glycation end products (AGEs), receptor of AGE (RAGE), HIF-1α, vascular endothelial growth factor (VEGF) and the levels of interleukin-1β(IL-1β), interferon-γ(IFN-γ), malondialdehyde (MDA) and total antioxidant capacity (T-AOC) were detected. Results: The FBG of diabetes group, mongolian drug group and cytokine group were higher than those of the the control group(P<0.05), and there was no significant difference among the three groups (P>0.05). Compared with the control group, the area of ulcer wound, the scope of unrepaired tissue under microscope, the expression level of AGEs, RAGE and the levels of IL-1β, IFN-γ, MDA in the wound tissue of the diabetes group increased, the level of T-AOC and expression levels of HIF-1α, VEGF of the diabetes group decreased (P<0.05). Compared with the diabetes group, the area of ulcer wound, the scope of unrepaired tissue under microscope, the expression level of AGEs, RAGE and the levels of IL-1β, IFN-γ, MDA in the wound tissue of the mongolian drug group and cytokine group decreased, the level of T-AOC and expression levels of HIF-1α, VEGF of the mongolian drug group and cytokine group increased (P<0.05) and the indexes of mongolian drug group were better than those of cytokine group. Conclusion: Mongolian drugs Hatagaqi-7 promotes ulcer wound healing of diabetes rats, and the inhibiton of AGEs and RAGE expression and the activaton of HIF-1 α is a possible molecular mechanism.
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Effect of Osteoking on lowering blood sugar and improving intestinal flora in db/db mice

dengshaoyou, zhaoyulan, wangpeijin, lirong, zhaohongbin, jiaojianlin, zhenghong

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Objective:To investigate the effects of Osteoking on hyperglycemia and regulating gut microbiota in db/db mice. Methods:The wild mice were used as the cntrol group and db/db mice were randomly into model group and Osteoking group. After intragastric administration for 12 weeks, Fasting blood glucose, serum glycosylated hemoglobin and insulin levels were measured , the changes of intestinal microflora were determined and functional pathways related to intestinal microflora in mice were predicted by 16S rDNA sequencing technology. Results:Compared with model group, Osteoking decreased fasting blood glucose (P < 0.01), serum glycosylated hemoglobin (P < 0.01), insulin resistance index (P < 0.01), and increased insulin content (P < 0.01) in db/db mice. Osteoking increased the abundance of beneficial bacteria of intestinal microflora, while decreased the abundance of harmful bacteria; the abundance of Marvinbryantia was increased. Osteoking alleviated the decrease of metabolism of D-arginine and D-ornithine, sphingolipid and galactose metabolism( P < 0.05), while inhibited lysine degradation, sulfur relay system and propanoate metabolism( P < 0.05). Conclusion:Osteoking has the effects of hypoglycemic properties and improving the intestinal microflora imbalance in db/db mice.
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Research progress on the role of autophagy in the pathogenesis of systemic sclerosis

lixin, sun xiaolin, wang yongfu

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【Abstract】 Systemic sclerosis (SSc) is an autoimmune disease characterized by vascular lesions and skin fibrosis, which can cause structural and functional damage to multiple organs. The pathogenesis of SSc is complex, which may be related to genetic, environmental factors and abnormal immune mechanisms. Autophagy is an evolutionarily conservative process of self degradation in the body, which can participate in the pathogenesis of body immunity and autoimmune diseases through a variety of pathways. This article mainly reviews the research progress on the role of autophagy in the angiopathy and fibrosis of SSc through regulating immune cells and mediating signal pathways.
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The role and mechanism of miRNAs in alcoholic liver injury in rats

congmeili

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Objective To investigate the role and mechanism of miRNAs in alcoholic liver injury in rats. Methods Randomly divided 30 male SD rats into model group and control group. The model group was gavaged with 56% liquor and the control group with distilled water for 8 weeks. The liver tissue was dissected. The miRNAs in the liver tissue were detected, analyzed and the target genes of differential miRNAs were predicted by rat miRNA chip. Gene Ontology (GO) and KEGG Pathway enrichment analysis were used to understand the function of differential miRNA target genes. Differential miRNA-mRNA-Pathway regulatory network was constructed using Cytoscape to further screen regulatory key miRNAs versus key pathways, qRT-PCR was performed on selected miRNAs for expression quantity validation analysis. Results: A total of 12 differentially expressed miRNAs (P < 0.05, fold change ≥ 2) were screened out, including 2 upregulated and 10 downregulated miRNAs by comparative analysis of microarray data between the model and control groups. GO classification annotation of differential miRNA target genes showed that there were close associations between differential miRNAs and biological functions such as antioxidant activity, metabolic process, biological regulation, cell killing, signal transduction, and enzyme regulatory activity. Differential miRNA target genes KEGG pathway analysis revealed that AMPK signaling pathway, PI3K Akt signaling pathway, Hippo signaling pathway, Wnt signaling pathway, cancer, autophagy, insulin resistance, Ras signaling pathway and other signaling pathways may play important regulatory roles in alcoholic liver injury lesions. The hub miRNAs and pathways screened by constructing the differential miRNA-mRNA-pathway regulatory network were mir-145-5p, mir-107-3p, mir-297, Hippo signaling pathway, cancer, PI3K Akt signaling pathway, AMPK signaling pathway, etc. The results of qRT-PCR showed that picking validation gene expression trend and gene chip results were consistent. Conclusion: In this study, we established a miRNA profile in alcoholic liver injury in rats, which suggests that mir-145-5p, mir-107-3p and mir-297 may play an important role in the process of liver alcoholic pathology.
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Osteopontin (OPN) activates the PI3K/AKT pathway via upregulating LGALS3BP in promotion of hepatoma cell migration

denglinlin, anriwen, zhaofangxin, linting, liucuihua, hongmei, wujianqiang, zhangxuan

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Abstract: Objective To investigate the effect and mechanism of osteopontin (OPN) on hepatoma cell migration through galectin 3 binding protein (LGALS3BP). Methods Human hepatoma cell lines SMMC-7721, SMMC-P (stably transfected with empty eukaryotic expression vectors) and SMMC-OPN (stably transfected with OPN gene) were cultured. The mRNA expression levels of OPN and LGALS3BP were detected by qRT-PCR. Western blot assay was used to analyze the relative expressions of OPN and LGALS3BP. The protein expression level of PI3K/AKT pathway, including p-PI3K, PI3K, p-AKT and AKT were detected by western blot. Wound healing assay was performed to explore the cell migration ability. After transfection with LGALS3BP-targeting small interfering RNA (si-LGALS3BP) and negative control small RNA (si-NC) into SMMC-OPN cells respectively, cell migration ability and the relative expression of PI3K/AKT pathway related proteins were detected. Results Compared with SMMC-7721 and SMMC-P, the migration ability of SMMC-OPN cells was significantly reinforced, and the expression of LGALS3BP was obviously up-regulated at both mRNA and protein. Meanwhile, the relative expression quantity of p-PI3K/PI3K and p-AKT/AKT proteins were significantly increased. Wound healing assay showed that the si-LGALS3BP could obviously suppress the migration ability of SMMC-OPN cells. Furthermore, the relative expression of p-AKT/AKT and p-PI3K/PI3K proteins in SMMC-OPN cells were significantly decreased after transfection with si-LGALS3BP. Conclusion OPN could activate PI3K/AKT pathway through up-regulating LGALS3BP expression in promoting hepatoma cells migration.
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Establishment method and effect evaluation of two common pressure uler rat models

liuyi, lixiaolei, liangxinpei, wangna, mashan, zhangxinping, jiarufu, zhangsu, lixian

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Objective : By comparing two different methods of establishing rat models of pressure uler, to explore a more suitable method for preparing animal models of pressure uler. Methods : 18 male SD rats were randomly divided into control group ( n = 6 ), model group A ( n = 6 ) and model group B ( n = 6 ). Control group : iodophor treatment was performed after hair removal at the simulated modeling site. Model A group : longitudinal compression was performed by simple deep tissue foreign body implantation ; model group B : transverse compression was performed by magnet compression method. The whole process time and each stage time of pressure uler model in each group were recorded. The general condition of rats was observed, and the molding rate, mortality rate and infection rate were compared. Results : The naked eye observed that the model A group and the model B group gradually appeared redness and swelling, ulceration, bleeding, exudation and necrosis. Comparison of the whole time of pressure uler in model group A and model group B : the difference between the two groups was statistically significant ( P0.05 ) ; the difference between the two groups was statistically significant ( P < 0.05 ). The difference between the two groups was statistically significant ( P < 0.05 ). There was significant difference between the two groups in stage IV ( P < 0.05 ). The mental and motor scores of the rats in the control group were significantly different from those in the model group A and the model group B ( P < 0.05 ). The general state of rats in model group A and model group B was significantly different, and the coat color was dim and the activity decreased. The model rate of rats in model A and model B was 100 %. The mortality and infection rate of model A group were higher than those of model B group, which were 33.34 % and 16.70 % respectively. Conclusion : Both methods can successfully prepare a four-stage model of pressure uler. The two methods have both commonalities and their own characteristics. The magnet compression method takes a short time, the rats are generally in good condition, and the mortality and infection rate are low. It is suitable for short-term intervention research ; the simple deep tissue foreign body implantation method takes a long time, requires rats to have a certain tolerance, has a high infection rate and a high mortality rate, and can be used in long-term observation of pressure uler rats.
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Research progress in the regulation of glutamate in traditional Chinese medicine in the treatment of depression

li chao

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Glutamate is a major excitatory neurotransmitter in the central nervous system and a potential neurotoxin. During the development of depression, there is an increase in glutamate concentration in the hippocampus, and when glutamate accumulates, it will cause serious damage to neurons and brain tissue, aggravating the depressive state. Therefore, glutamate accumulation may be an important mechanism for depression. Astrocytes, glutamate transporters and glutamate receptors play important regulatory roles in the concentration of glutamate. This article reviews the mechanism of action of traditional Chinese medicine therapy on the treatment of depression by regulating astrocytes, glutamate transporters, and glutamate receptors, and provides new ideas for exploring the treatment of depression by traditional Chinese medicine.
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To explore cognitive differences among dogs with different sociability

song meng yu, guo yi jun, zhao xue rong, bai jing, zhou zi juan, wang jing yu

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Objective:Exploring whether there are differences in the cognitive abilities of socially different Labradors. Methods:The Dog Mentality Assessment (DMA) test created by the Swedish Working Dog Association was modified to use 12 behavioral variables from five subtests of the DMA test: Social contact, Play I, Distance-play, Ghosts and Play II to assess the sociability of the dogs. According to the scoring criteria,49 Labradors provided by The China Guide Dog Training Centre In Da Lian was scored on the social behavioral variables, which were classified into high (n=15) and low (n=34) sociability groups using cluster analysis. A new system for testing canine cognitive ability was developed based on Bray et al.'s Dog Cognitive Development Battery (DCDB), which tests different domains of cognitive ability such as social cue use, unsolvable task, inhibitory control, cognitive flexibility, working memory and multi-step problem solving task, and the dogs' behavioral performance and duration of the test were recorded. Statistical analysis was performed to determine whether there were differences in the cognitive abilities of socially diverse dogs. Results:Dogs in the high and low social subgroups differed significantly on behavioral variables in the unsolvable task, the inhibitory control test and the multi-step problem solving task. In the unsolvable task, dogs in the high social grouping average looked at people time for significantly longer than dogs in the low social grouping (P=0.008) and average looked at people for significantly less latency time than dogs in the low social grouping (P=0.0001). In the inhibitory control, dogs in the high social group chose correctly significantly more than dogs in the low social group (P=0.034) and chose for significantly less time than dogs in the low social group (P=0.039). In the multi-step problem solving task, dogs in the high social group successful completion number of stakes significantly higher than dogs in the low social group (P=0.044); the percentage of operation pale time was significantly lower than dogs in the low social group (P=0.05); the average latency time to solve bone task was significantly higher than dogs in the low social group (P=0.037); and the percentage of operation bone time was significantly lower than dogs in the low social group ( P=0.038). On tests involving manipulable apparatus, dogs in the high social group spent more time looking at people than dogs in the low social group and less time manipulating the apparatus than dogs in the low subgroup, but there were no statistically significant differences (P>0.05). Conclusions:High sociability labradors showed greater cognitive ability,they were more able to suppress impulses during the test, were more able to complete multi-step problem solving task and were more inclined to change strategies to seek new cues from people rather than obsessing over manipulating the apparatus when they were unable to solve a problem.
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Construction of a prognostic risk marker of colon adenocarcinoma based on weighted gene co-expression network and its clinical significance

liyihui

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Objective Due to the poor prognosis of colon adenocarcinoma (COAD) patients, it is necessary to screen prognosis-related genes in COAD and establish a new prognostic risk assessment model. Methods COAD-related data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) were used as the training set and the validation set, respectively. Weighted gene co-expression network analysis (WGCNA)， Cox regression model and Least Absolute Selection and Shrinkage Operator (LASSO) regression analysis were used to screen prognosis-related genes of COAD and construct a prognostic model. Receiver Operating Characteristic (ROC) curve was combined with survival curve to verify the accuracy of the model, and a nomogram was established. The patients were divided into two groups according to the median value of risk score. The immune cell proportion score (IPS) was used to evaluate the immunotherapy response of the two groups. Results A total of 15 feature genes were screened. The area under the ROC curve (AUC) in the predictive model of COAD patients was >0.6, and the survival rate of high-risk group was significantly lower than that of low-risk group (P<0.05, suggesting good distinguishing ability for high- and low-risk COAD patients. Patients in the low-risk group had a higher IPS (P=0.026), indicating a better response to immunotherapy. Conclusions The model developed for COAD in this study has a good ability to predict the survival of people at high and low risk of COAD.
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Quality Evaluation for Animal Studies on Acupuncture for Glaucoma

lijiaxian, lianglina, 李亚敏, xukai, huangziyang, lixiaoyu, jinyu, zhouwei

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Objective To evaluate the quality of animal studies on acupuncture for glaucoma by the SYRCLE’s risk of bias tool, ARRIVE 2.0 guidelines and GSPC checklist. Methods Databases of CNKI, VIP, Wanfang, Sinomed, PubMed, Web of Science, Embase, and Cochrane Library were conducted to find animal research articles on acupuncture for glaucoma. Risk of bias was assessed for included studies using the SYRCLE’s tool, and the reporting quality was evaluated using the ARRIVE 2.0 guidelines and GSPC checklist, statistical analysis was performed by Excel and SPSS software. Results Thirty articles met the inclusion/exclusion criteria and were included in the final analysis. 6 of the 10 items of the SYRCLE’s tool had a low-risk rate of <50%, and the non-low-risk items focused on selectivity bias, implementation bias, and measurement bias. 12 of the 22 essential sub-items of the ARRIVE 2.0 guidelines had a low-risk rate of <50%; 9 of the 16 recommended sub-items had a low-risk rate of <50%; 12 of the 19 subentries of the GSPC list had a low-risk rate of <50%, and randomization, blinding, thical statement, housing and husbandry, animal care and monitoring, protocol registration were non-low-risk items in the ARRIVE 2.0 guidelines and GSPC list. Conclusion The quality of methodology and experimental reportings in animal studies on acupuncture for glaucoma are generally low, and the descriptions of several items are not yet complete, which affects the readers' judgment on whether the animal studies can be further translated into clinical studies. It is advised to further promote the SYRCLE’s tool and reporting guidelines for animal experiments, to enhance the design, performance, and reporting of animal experiments, ensure the reproducibility of experiments and results, and provide reliable evidence for the translation of results to the clinic.
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miR-181a-5p overexpression in the small intestine in a mouse model of subcutaneous transplantation of oral cancer

wuxuehai

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[Abstarct] Objective By detecting changes in metabolites and metabolic pathways in the small intestine of mice with subcutaneous transplantation of oral cancer, the effects of overexpression of miR-181a-5p on metabolites and metabolites in the small intestine of mice with subcutaneous transplantation of oral cancer were analyzed. Methodes Three groups existed in the experiment: the Control group, the Negative control group, and the Over expression of miR-181a-5p group in the experimental group. To construct a subcutaneous transplantation tumor mouse model of oral cancer, different groups of treated cell suspensions were subcutaneously injected into the right point and upper location of the groin of M-NSG severely immunodeficient female mice. The pathogenic changes in each group were identified while additionally following the changes in the mice's body weight and small intestinal tissues using HE staining. By using tandem Orbitrap mass spectrometry and ultra-high performance liquid chromatography-tandem time-of-flight mass spectrometry, the metabolites in the small intestine of mice in the NC group, OE group, and Control group have been detected. By pre-analyzing the original data and quality rating sample data, XCMS was able to assess which metabolites were different between the Control group and NC group and between NC group and OE group. To establish the unique metabolic pathways, KEGG enrichment analysis was used. Results A total of 170 distinct metabolites were found in the small intestinal tissues of the Control and NC groups. Choline metabolism, alanine, aspartate, and glutamate metabolism, GABA synaptic metabolism, glycerophospholipid metabolism, cAMP signaling route, cancer center carbon metabolism, and niacin and niacin amine metabolic pathways are important signaling pathways for metabolite enrichment. In the NC group, 16 distinct metabolites with VIP values larger than 2 were found in the small intestine of mice compared to the OE group that overexpressed miR-181a-5p. Glycerin phosphoylcholine, palmitic acid, 3-hydroxybutyryl carnitine, -hydroxybutyric acid, etc. are example of the metabolites which significantly vary. The primary raised metabolism path is the one for choline. Conclusions Mice's small intestine suffered slight changes as a result of subcutaneous transplantation of oral cancer, with the greatest effect in the metabolites critical in energy metabolism. The choline metabolic path was the pathway that selected absolutely metabolites in the small intestine of mice with the subcutaneous grafts of oral cancer.
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The effect of cobalt dichloride regulating inflammatory response and insulin resistance in 3T3-L1 adipocytes based on HIF-1α/ autophagy pathway

yuexinxin, Fu Yang, Li Yi Rang, Yin xiao yan, Yu Fei, Fu quan wei

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Objective: To investigate the effect of hypoxia inducer cobalt chloride (CoCl2) on autophagy in 3T3-L1 adipocytes. Methods: 3T3-L1 adipocytes were cultured and induced to become mature adipocytes. CoCl2 was used as an inducer of hypoxia in vitro. Mature adipocytes were divided into control group, CoCl2 intervention group with different concentrations and different time. According to the above results, 150μmol/L cobalt chloride was selected to intervene adipocytes for 0h,12h,24h and 48h, respectively. Then the cells were collected for related tests. MTT assay was used to detect cell survival in each group. The expressions of HIF-1α, autophagy-related protein LC3Ⅱ, Beclin 1 and glucose transporter Glut-1 were analyzed by Western blot. The level of autophagy activity was detected by immunofluorescence.The levels of TNF-α and IL-6 in the supernatants of adipocytes were measured by ELISA. Results: The survival rate of adipocytes was decreased after treatment with 150μmol/L CoCl2 for 24 hours. The expression levels of HIF-1α, LC3-Ⅱ, Beclin 1 and Glut-1 proteins were significantly increased in 24h. Autophagy activity level was significantly increased in 24h. The secretion levels of inflammatory cytokines TNF-α and IL-6 were not significantly increased in 24h. Conclusion: Autophagy can be moderately activated by 150μmol/L CoCl2 intervention in adipocytes for 24 hours. The activation of autophagy can be activated in a HIF-1α-dependent manner, which plays a role in protecting adipocytes from inflammatory damage and improving insulin resistance.
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Progress in microglia-astrocyte interactions and their mediated neuroinflammation in Alzheimer's disease

HU Xin, WANG Qian, ZHANG Chen-xi, ZHENG Hui-hui, LI Peng-yang, ZHAO Hong-ye, DENG Feng-chun

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Alzheimer's disease (AD) is an aggressive neurodegenerative disease whose pathogenesis is hitherto unknown. Neuroinflammation is a chronic inflammatory response in the central nervous system (CNS) activated by microglia and astrocytes that is difficult to subside autonomously and is associated with multiple inflammatory factors and the blood-brain barrier (BBB). Recent studies have shown that neuroinflammation has become the third major pathological feature in AD after β-amyloid (Aβ) deposition and neurogenic fiber tangles (NFTs). In this paper, we summarize and analyze microglia and astrocytes and their interaction, and organize and discuss the role of microglia-astrocyte interaction in neuroinflammation and AD. In order to provide a reference for the involvement of microglia and astrocytes in the pathological alterations of neuroinflammation in AD.
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Research progress of miRNA in neuroprotection of ischemic stroke

lihongyu, lanrui

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Ischemic stroke is a cerebrovascular disease with high disability and mortality, and can be life-threatening in severe cases, which has a heavy social and economic burden worldwide. The etiology and pathological process of ischemic stroke are mediated by a variety of molecular processes, and some of these molecular mechanisms are dynamically regulated after transcription. Increasing evidence has shown that Micro-ribonucleic-acid (miRNA), as an important mediator of post-transcriptional gene silencing, plays a crucial role in gene expression and the pathological process of ischemic stroke. In this review, we present the neuroprotective effects of mirnas in different mechanisms of ischemic stroke. Since the promotion or inhibition of miRNA expression through specific drug and non-drug therapy may be beneficial to the recovery of ischemic stroke, the clinical diagnosis and treatment of miRNA in ischemic stroke are also discussed in detail in this paper, aiming to provide a certain reference for clinical and basic research in this field.
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Research progress on the effect of miRNAs on liver metastasis of digestive system tumors

Yangsiqi, jinming, zouqinling

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Liver is the most common organ that tumors spread to, and expression of miRNA is very important in the process of liver metastasis. In this study, research progress of related miRNAs in regulating liver metastases from digestive system malignant tumors was collated and analyzed. Through searching related literature, this paper provides an introduction to the role of miRNAs in liver metastasis of colorectal cancer, gastric cancer, pancreatic cancer and gallbladder cancer, which helps with the diagnosis, treatment and research of tumor liver metastasis.
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Establishment of chronic alcoholic brain injury model in mice

Cai Yu

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【Abstract】 Objective To establish an effective and reliable chronic alcoholic brain injury model in mice. Methods C57BL/6J mice were randomly assigned into the control group and the model group. Mice in the model group were given free access to 5% (v/v) alcohol in drinking water, and were intragastrically administered with 28% (v/v) alcohol. The gavage dosage increased gradually over the first two weeks (from 0 to 6 g/kg body weight), and remained at 6 g/kg body weight for the subsequent four weeks. Mice in the control group were provided with normal water and given same amount of saline via gavage. At the end of the experiment, the cognitive function and motor ability of mice were evaluated through behavioral tests. The morphological changes of brain tissue of mice were examined by histopathological staining. Results Compared to the control group, mice in the model group showed cognitive impairments and motor dysfunction in the behavioral tests. The pathological examination of the brain tissue from the model group mice showed morphological damage and cell necrosis in the hippocampus. Conclusions The mouse model of chronic alcoholic brain injury was successfully and effectively established in this study, providing a valuable tool for investigating the underlying mechanisms and potential therapeutic interventions for chronic alcoholic encephalopathy.
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Molecular mechanism and prognosis of patients with HBV infection with DLBCL

Yuanherui, guopengxiang

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In recent years, hepatitis B virus (HBV) infection patients with diffuse large B cell lymphoma (DLBCL) have shown an upward trend, and its etiology is complex and treatment is difficult, so it has received extensive attention from scholars at home and abroad. Based on the review and analysis of the research of domestic and foreign scholars, this paper further discusses the mechanism of the occurrence and development of DLBCL caused by HBV infection and the clinical prognosis of related patients, and finally finds that at the genomic and transcriptome levels, HBV may mainly induce the changes of BCL6, FOXO1, ZFP36L1 and other genes, and activate various regulatory genes through HBV's X protein, thereby inducing clonal proliferation of lymphocytes and eventually forming lymphoma. For the clinical prognosis assessment, the clinical prognosis assessment mainly analyzes and compares the patient's age of onset, sex, organ involvement, international prognostic index (IPI), lactate dehydrogenase (LDH) level, proliferation index (Ki-67), bcl-2, bcl-6, inflammatory index and other factors, aiming to put forward a theoretical basis for the clinical diagnosis and treatment of DLBCL and basic research.
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Study on the mechanism of lncRNA SNHG16 regulating the resistance of hepatoma cells to sorafenib by miR-570

liuyang, Fan Wei, Ding Jie

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Objective: To explore the mechanism of long non-coding RNA SNHG16 (Long non-coding RNA small nucleolar RNA host gene16, lncRNA SNHG16) to anti-liver cancer cell resistance by regulating minimal RNA-570 (miR-570). Methods: The expression of lncRNA SNHG16 and miR-570 of HepG 2 and HepG 2-R cells in human normal liver and hepatoma cells was measured by real-time fluorescence RT-PCR, cell proliferation, apoptosis and invasion were measured by MTT assay, FACS and Transwell test, and cell expression changes of CyclinD1, P21MMP-9 and MMP-2 were determined by Western Blot assay. Results: Compared with normal hepatocytes, lncRNA SNHG16 expression was increased and miR-570 expression was decreased in hepatoma cells (P<0.05). Compared with HepG2-P group, LncRNA SNHG16 and IC50 values were increased in HepG2-R group, and the inhibition rates of miR-570 and HepG2-R cells were decreased at Sorafenib concentrations of 1, 2, 4, 8, 16μmol/L (P<0.05). HepG2-R pcDNA SNHG16 as overexpression group, lncRNA SNHG16 expression was significantly increased (P<0.05), and compared with HepG2-R pcDNA group, In HepG2-R pcDNA SNHG16 group, the number of migrated cells, the expressions of CyclinD1, P21, MMP-9 and MMP-2 were decreased, while the expression of inhibition rate, apoptosis rate and P21 were increased (P<0.05). Compared with HepG2-R anti-miR-NC group, miR-570 level in HepG2-R anti-miR-570 group was decreased (P<0.05), and compared with HepG2-R anti-miR-NC group, HepG2-R anti-miR-570 group decreased the levels of CyclinD1, MMP-9 and MMP-2, and increased the levels of inhibition rate, apoptosis rate and P21 (P<0.05). Dual luciferase reporting experiment showed that compared with miR-NC group, miR-570 reduced the luciferase activity of WT-SNHG16 (P<0.05), but had little effect on the luciferase activity of T-SnHG16 (P>0.05). Overexpression of lncRNA SNHG16 decreased the expression of miR-570 in HepG2-R cells (P<0.05). Compared with HepG2-R pcDNA SNHG16 miR-NC group, In HepG2-R pcDNA SNHG16 miR-570 group, the number of migrated cells, the levels of CyclinD1, MMP-9 and MMP-2 were increased, while the levels of inhibition rate, apoptosis rate and P21 were decreased (P<0.05). Conclusion: By regulating the drug resistance of HepG2-R hepatoma cells, the mechanism is related to the regulation of miR-570 by lncRNA SNHG16, and it can be used as a new target for drug-resistant HCC cell therapy.
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Study on the Mechanism of Hyperuricemia combined with Nonalcoholic Fatty Liver based on PI3K/Akt/NF-kB

gongxiaohong, lihuan

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Abstract: Objective: To study the pathogenesis of hyperuricemia combined with nonalcoholic fatty liver disease (HUA-NAFLD) based on PI3K/Akt/NF-kB signaling pathway. Methods: 64 SD rats were randomly divided into blank group, HUA group, NAFLD group, and HUA-NAFLD group, 16 rats in each group. The samples were collected at the end of the 8th and 12th week, respectively. The serum biochemical indexes of the rats were detected; The pathological changes and lipid deposition in liver tissue were observed by hematoxylin-eosin staining (HE) and Oil Red O staining; the expression levels of PI3K/Akt/NF-kB signaling pathway-related proteins in liver tissue were detected by Western blot. Results: Compared with the other three groups, the liver index of the rats in the HUA-NAFLD group was significantly increased (P<0.05). Compared with the blank group, the levels of UA and LDL in the HUA group were increased, the levels of HDL in the NAFLD group were decreased, the levels of UA, CHOL, TG and LDL in the HUA-NAFLD group were increased, and the levels of HDL were decreased (P＜0.05); Compared with the HUA-NAFLD group, the levels of CHOL, TG and LDL were decreased in the HUA group, and the levels of UA, TG and LDL in the NAFLD group were decreased (P＜0.05). The results of HE and oil red O staining showed that compared with the other three groups, rat liver cells in the HUA-NAFLD group had a large number of fat vacuoles, blurred liver cord structure and more severe lesions. The WB results showed that compared with the blank group, the phosphorylation levels of AKT and p65 in the NAFLD group were significantly increased, and the phosphorylation levels of AKT, PI3K, p65 and IKKβ in the HUA-NAFLD group were significantly increased, and compared with the HUA-NAFLD group, the phosphorylation levels of AKT and p65 in the HUA-NAFLD group decreased significantly(P<0.05). The phosphorylation level of IKKβ decreased significantly in the HUA group, and compared with the HUA group, the phosphorylation level of p65 in the NAFLD group increased significantly (P<0.05). Conclusion: Compared with the single disease group, the HUA-NAFLD group has more abnormal biochemical indexes and more severe liver lesions. The PI3K/Akt/NF-KB signaling pathway may play an important role in the pathogenesis of HUA, NAFLD and HUA-NAFLD.
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Study on Allicin improves human peritoneal mesenchymal cell-mesenchymal transformation induced by high glucose through the JAK2/STAT3 signaling pathway

Gan Linwang, Li Qiancheng, Gao Lichao, Liu Qi, Li Ying, Wang Yujie, Ou Santao

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Objective To investigate the mechanism of allicin in improving human peritoneal mesenchymal cell-mesenchymal transformation induced by high glucose. Methods human peritoneal mesothelial cells (HPMCs) were cultured and divided into two groups. Group 1: ①Control group; ②8.5 mM D-glucose induced group (8.5 mM DG group); ③17 mM D-glucose induced group (17 mM DG group); ④34 mM D-glucose induced group (34 mM DG group); ⑤68 mM D-glucose induced group (68 mM DG group). Except the control group, the other groups were induced with D-glucose of 8.5 mM, 17 mM, 34 mM and 68 mM, respectively, for 48 h. Group 2: ① control group; ②34 mM D-glucose induced group (HG group); ③34 mM D-glucose + low dose allicin induction group (AL-L group); ④34 mM D-glucose + medium dose allicin induction group (AL-M group); ⑤34 mm-glucose + high-dose allicin induction group (AL-H group); ⑥34 mM D-glucose + JAK2 inhibitor induction group (JAK2 group). HG group was induced with 34 mM D-glucose for 48 h, AL-L group, AL-M group and AL-H group were pretreated with 34 mM D-glucose for 6h, and then induced with 10 ng/mL, 20 ng/mL and 40 ng/mL allicin for 48 h, respectively. JAK2 group was pretreated with 1 μmol/L AG490 for 6 h and induced with 34 mM D-glucose for 48 h. The contents of IL-6, TNF-α and IL-1β in HPMCs supernatant were determined by Elisa. CCK-8 was used to detect cell proliferation and morphology. The expressions of JAK2, p-JAK2, STAT3, p-STAT3, N-cadherin, E-cadherin, Vimentin, α-SMA, MCP-1, p65 and p-p65 proteins were detected by Western blot. Results Compared with the control group, the relative survival rate of HPMCs in the high glucose induced group was significantly reduced (P<0.01), and cell morphology was abnormal, the expressions of α-SMA, N-cadherin and Vimentin that promote epithele-mesenchymal transdifferentiation were significantly up-regulated, and the expression of E-cadherin, which inhibits EMT, was significantly down-regulated. JAK2/STAT3 signaling pathway was activated, leading to the occurrence of EMT (P<0.01). Allicin can significantly promote the proliferation of HPMCs induced by high glucose, restore abnormal cell morphology, regulate the level of EMT-related proteins, and improve the epithelial-mesenchymal transdifferentiation of HPMCs. Compared with the high glucose induction group, the pro-inflammatory cytokines IL-1β, IL-6 and TNF-α of HPMCs in allicin treatment group were significantly decreased, and the expressions of pro-inflammatory proteins p-p50 and MCP1 were significantly down-regulated, indicating that allicin could improve the inflammation caused by EMT. Conclution Allicin can improve EMT and inflammation induced by high glucose by inhibiting JAK2/STAT3 signaling pathway to regulate the levels of markers of EMT, inflammatory signaling proteins and inflammatory factors.
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Influence of hyperoside on autophagy in rats with nephrotic syndrome by regulating AMPK/mTOR/ULK1 signaling pathway

kongloujiao, wangxin, liujing, guoxiaoyang, xuemingwei

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Objective To investigate the influences of hypericin (Hyp) on renal autophagy and AMPK/mTOR/ULK1 pathway in nephrotic syndrome (NS) rats. Methods Thirty-two 6-week-old SD rats were grouped into normal group (N group), NS group, Hyp group (60 mg/kg Hyp), Hyp AMPK inhibitor group (Hyp CC group) (60 mg/kg Hyp group) 0.2 mg/kg CC), 8 per group. After administration, an automatic analyzer was applied to detect the levels of 24-h urine total protein (UTP), blood urea nitrogen (BUN), serum creatinine (Scr) and albumin (ALB); HE staining and TEM observation were applied to observe renal pathological morphology and ultrastructure; Western blot was applied to detect the expression of autophagy, podocyte and AMPK/mTOR/ULK1 pathway proteins in kidney; immunofluorescence staining was applied to visualize the localization of autophagosomes and podocytes. Results Compared with the N group, the glomerular volume of the NS group increased, the renal tubules atrophied or partially disappeared, and the basement membrane thickened; UTP, BUN, Scr, basement membrane thickness, foot process width and the ratio of p-AMPK/AMPK were obviously increased (P<0.05), the protein levels of ALB, LC3-II/I, Beclin-1, Atg5, Atg7, NPHS2, the relative fluorescence intensity of NPHS2 and Beclin-1, and the ratios of p-AMPK/AMPK and p-ULK1/ULK1 were obviously decreased (P<0.05). Compared with NS group, Hyp treatment was able to improve glomerular morphology, decrease UTP, BUN, Scr, basement membrane thickness, foot process width and ratio of p-AMPK/AMPK (P<0.05), increase protein levels of ALB, LC3-II/I, Beclin-1, Atg5, Atg7, NPHS2, the relative fluorescence intensity of NPHS2 and Beclin-1 and the ratios of p-AMPK/AMPK and p-ULK1/ULK1 (P<0.05). AMPK inhibitor group CC could attenuate the autophagy-promoting and kidney-protecting effects of Hyp. Conclusion Hyp may enhance the autophagy activity of renal cells and attenuate renal pathology such as podocyte injury in NS rats by activating the AMPK/mTOR/ULK1 pathway.
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Study of core symptom impact on baicalein in an animal model of attention deficit hyperactivity disorder SHR rat

zhang yongting, Zhou Rongyi, Ma Bingxiang, Wu Chenlei, Xie Xinyue, Ding Xueying

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Objective To explore the efficacy and potential mechanism of baicalin in regulating the core clinical symptoms of ADHD through the Morris water maze test and The open field test. Methods Thirty SHR rats were randomly divided into model group, methylphenidate hydrochloride(MPH) group, baicalin group, baicalin + tetrabenazine group and MPH + tetrabenazine group, with 6 rats in each group. Another 6 WKY rats were used as normal control group. The rats in the MPH group (1.5 mg/kg) and the baicalin group(150 mg/kg) were given the corresponding drugs (1 mL/100 g) by gavage, and those in the normal control group and the model group were given an equal volume of normal saline by gavage . In addition to the corresponding drug gavage,the rats in the MPH+tetrabenazine group and the baicalin+tetrabenazine group were given intraperitoneal injection of tetrabenazine(3 mg/kg) according to body weight (0.5 ml/100 g).The course of treatment was 4 weeks for all groups. Open field and Morris water maze experiments were carried out at the specified time, and the experimental results were recorded and analyzed Results In the open field experiment, the total distance and average speed in the MPH group and baicalin group were significantly lower than those in the model group (P < 0.05), and there was no significant difference between the two groups (P > 0.05);In the open field experiment, the total distance and average speed in the baicalin + bubenazine group were significantly lower than those in the model group (P < 0.05), and obviously higher than those in the baicalin group. In the water maze test, the latency of baicalin + bubenazine group was significantly shorter than that in the model group (P < 0.05), and significantly longer than that in the baicalin group (P < 0.05). The percentage of movement distance and stay time in the target quadrant in the baicalin + bubenazine group were obviously higher than those in the model group. It was significantly lower than that in baicalin group (P < 0.05).Conclusion Baicalin can control the core symptoms of hyperactivity, impulse and inattention in SHR rats, and its curative effect may be related to the regulation of dopamine vesicle transport.
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Study on the mechanism of ethyl acetate extract of Liujunzi Decoction on the energy metabolism of EC9706 cells in CAFs conditioned medium

Chen Xing, Lou Xiangyu, Shang Yiwan, Zhou Zhexu, Liu Yang, Liu Yaru, Hu Xiaobo, Chen Yulong

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Objective: To explore the molecular mechanism of ethyl acetate extract of Liujunzi Decoction(EAELD) on energy metabolism of esophageal cancer EC9706 cells in conditioned medium of cancer-associated fibroblasts (CAFs). Methods: Methyl thiazol tetrazolium (MTT) assay was used to detect the effect of EAELD on the proliferation activity of EC9706. The effects of EAELD on lactate and glucose in the supernatant of EC9706 cells in CAFs conditioned medium were detected by colorimetry. seahorse system energy metabolism analysis system was used to detect the effect of EAELD on energy metabolism of EC9706 cells in CAFs conditioned medium. Real-time fluorescent quantitative PCR (q-PCR) and western blotting were used to detect the mRNA and protein expression of energy metabolism-related molecules.. Results: Compared with DMEM, except for the 10μg/mL group,EAELD had a significant inhibitory effect on the proliferation of EC9706 cells (P < 0.05). The inhibitory concentration (IC30) of 25μg/mL and half inhibitory concentration (IC50) of 40μg/mL were selected as the low and high dose groups for subsequent experiments. Among EC9706 cells cultured by CAFM, both low-dose and high-dose EAELD groups could significantly reduce Non-mitochondrial oxygen consumption, Basal respiration value, Maximum respiration value, Oxygen consumption of ATP synthesis, Spare respiration capacity, Basal glycolysis, Compensative glycolysis and glycolysis potential (P <0.01). Decreased the lactate content of EC9706 cells (P <0.01), down-regulated the mRNA expression of GLUT1 (P <0.05, P <0.01), down-regulated the protein expression of p-PKM2, HK2, PKM2 and MCT1 (P <0.01); The high-dose EAELD group could down-regulate the Mitochondrial oxygen consumption and basal use The glycolytic ratio of EC9706 cells (P <0.05), reduce glucose uptake of EC9706 cells (P <0.05), down-regulate the protein expression of p-PKM2 and GLUT1 (P <0.01, P <0.05); The low dose group of EAELD could down-regulate the mRNA expression of MCT1 (P <0.05). Conclusions:EAELD can interfere with the energy metabolism of EC9706 cells in CAFs conditioned medium, and its mechanism may be related to the regulation of HK2, PKM2, GLUT1, MCT1 and MCT4 mRNA and protein expression.
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Application characteristics of animal model of osteosarcoma based on data mining

yushuaike, luomaoli, wanglianrui, zhoutianbao, baili, miaomingsan

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Objective To summarize the key points of animal modeling of osteosarcoma, and to provide reference and suggestions for improving the modeling methods and evaluation indexes.Methods The database was established by searching the relevant literature on the animal model of osteosarcoma in CNKI, Wanfang database and PubMed. The species of experimental animals, gender, modeling methods, types of cancer cell lines and detection indicators were summarized, and the database was established for statistical analysis. Results A total of 284 literatures were included. Statistical analysis found that BALB / c-nu / nu nude mice were preferred in osteosarcoma model animals(227 cases，75.17%), followed by SD rats (20 cases, 6.62%). Subcutaneous cell fluid transplantation in the back (66 cases, 21.85%), subcutaneous cell fluid transplantation in the axils (55 cases, 18.21%) or in situ cell fluid transplantation (51 cases, 16.89%) were used as modeling methods. Human MG-63 cells (100 cases, 33.11%) and mouse UMR-106 cells (39 cases, 12.91%) were selected as the cancer cell lines.The most detected indexes were tumor tissue apparent index (238 cases, 83.80%), tumor tissue HE staining (129 cases, 45.42%), Animal apparent indicator (94 cases, 33.10%)，tumor tissue immunohistochemistry (89 cases, 31.34%), etc. Conclusions At present, osteosarcoma BALB / c-nu / nu nude mice aged 4 to 6 weeks are used as experimental animals, and human MG-63 cell heterotopic transplantation (back and axillary transplantation) is used to establish the animal model, and the detection indexes of osteosarcoma are comprehensively evaluated by animal apparent index, tumor apparent index and tumor histopathology. It is suggested to select serum biochemical index, apparent index of tumor tissue as well, HE staining of tumor tissue and immunohistochemistry of tumor tissue to evaluate the model. However, there is still a lack of animal model preparation and evaluation criteria with high clinical consistency. In this paper, the advantages and disadvantages are summarized through literature mining and data analysis, in order to provide reference for the establishment of a good OS model and better application to OS mechanism research and new drug development.
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Effects of moderate intensity and high intensity intermittent exercise on myocardial mitochondria autophagy in mice with nonalcoholic fatty liver disease

he miao, li jia hang, liu xin, yang wei, wu liang wen, fan jing jing

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Objective To investigate the effects of moderate aerobic exercise and high intensity intermittent exercise on myocardial mitochondria autophagy in mice with non-alcoholic fatty liver disease and its possible mechanism. Methods Forty 3-week-old male C57BL/6J mice were randomly divided into normal feeding group (Chow group, n=10) and high fat feeding group (HFD group, n=30). At week 18, those whose body weight in HFD group exceeded 20%~30% (including 20%) of the ordinary diet group were judged as obese mice (n=26). Two mice were randomly selected for liver oil red O staining to confirm the successful establishment of NAFLD mouse model. Sixteen NAFLD mice were randomly selected and divided into moderate intensity aerobic exercise group (MICT group) and high intensity intermittent aerobic exercise group (HIIT group), with 8 mice in each group. The two groups were given exercise training for 8 weeks, respectively, and the samples were weighed after intervention. Masson staining was used to observe myocardial fibrosis. The ultrastructure of myocardial cells was observed by transmission electron microscopy. Mitochondrial autophagy and mitochondrial biogenesis were detected by Western Blot. Results ⑴ Compared with Chow group, body weight and heart index in HFD group were significantly increased and decreased. Compared with HFD group, the body weight of MICT and HIIT group increased significantly, and the heart index of MICT group increased. (2) Masson results showed that compared with Chow group, the content of collagen fibers in myocardium in HFD group was significantly increased, and the myocardial fibers were disorganized and broken under electron microscope. The morphology of myocardium was disorganized, mitochondria were swollen, crists were broken and blurred, and lipid droplets were included. Compared with HFD group, the myocardial collagen fiber content in MICT and HIIT groups was significantly reduced, the myocardial fiber arrangement was slightly recovered under transmission electron microscopy, the Z-line was clearly visible, the degree of mitochondrial degeneration was slightly improved, and the lipid droplets were also slightly reduced. Among them, the improvement effect of MICT group on the cardiac tissue structure was better than that of HIIT group. (3) Western Blot results showed that compared with Chow group, the expression levels of PINK1 and Beclin1 in myocardial tissue of HFD group had no significant changes, while the expressions of Parkin, LAMP1 and PGC-1α were significantly decreased (p<0.01). p62 protein expression and LC3-II/LC3-I ratio were significantly increased (p<0.05, p<0.01); Compared with HFD group, the expression levels of PINK1 and Beclin1 in MICT and HIIT groups were not significantly changed, while the expression of PGC-1α was up-regulated, and the expressions of Parkin and LAMP1 in MICT group were significantly increased (p<0.05). p62 protein expression and LC3-II/LC3-I ratio were significantly decreased (p<0.05, p<0.01), Parkin and LAMP1 expression levels were up-regulated, LC3-II/LC3-I ratio and p62 protein expression were significantly decreased in HIIT group (p<0.05, p<0.01). Conclusion Different forms of aerobic exercise can effectively ameliorate myocardial structural and functional injury in NAFLD mice, which may be through stimulating the autophagy flux of mitochondria in cardiomyocytes, activating autophagy and restoring the normal autophagy function of cells, so as to ameliorate myocardial cell damage, and moderate continuous aerobic exercise has better improvement effect.
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Exploring the Management Innovation Mechanism of Emergency Science and Technology Research Projects in the Medical Field

CHEN Yujun, SU Meiyangyi, WANG Qingxuan, GAO Ran

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Objective The emergency technology research project highlights the two key aspects of "emergency" and "research", which are how to effectively achieve the goal results.Organizations that undertake such projects need to develop reasonable project management mechanisms to ensure the successful implementation of emergency technology research projects.This article aims to investigate the current problems in the management of emergency technology research projects in the medical field through research, analyze possible improvement measures, and improve the efficiency and quality of scientific research management.Methods This article combines the author's practical experience, investigates the current status of scientific research management in relevant units, and conducts questionnaire surveys on the management aspects that are most concerned by scientific management and researchers.Based on the problems reflected in the survey, experts are organized to discuss and demonstrate.Results Through the research, it is found that: 1. At present, there are few management norms for emergency technology research projects;2. The most concerned issue for scientific researchers is administrative approval and project funding;3. The most concerned issue for scientific management personnel is how to meet the management requirements of higher-level units and the needs of scientific researchers under the premise of legal compliance.Conclusion Emergency technology research projects have their own unique characteristics compared to conventional technology projects. Management optimization can be carried out in terms of project approval, fund use, resource allocation, and safety. This study provides innovative solutions for the management of emergency technology research projects, and provides useful experience and reference for various scientific research units in managing such projects.
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Effects of compound active tea of Lithocarpus litseifolius on uric acid and renal function in mice with hyperuricemia nephropathy

陈, zengyanan, DUXIAOLANG, MUZEJING, liaochengdong, zhangchanghua, caolan

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Abstract：Objective To explore the effect of compound active tea of Lithocarpus litseifolius on uric acid and kidney function on mice with hyperuricemia nephropathy , and to provide experimental basis for the development of hyperuricemia nephropathy drugs and functional food. Methods The mouse model of hyperuricemia nephropathy was established by potassium oxyoxide with adenine. Mice were randomly divided into normal group, model group, benbromarone positive drug group (10 mg?kg-1?d-1), and Compound active tea of Lithocarpus litseifolius high,middle, low-dose groups (10g?kg-1?d-1,3.33g?kg-1?d-1,1.11g?kg-1?d-1).1h after the last dose, urine protein (UP) was measured by CBB method,urea nitrogen (UUN) was measured by the urease method;Blood was collected for uric acid (UA) by enzyme ratio method and urea nitrogen (BUN) by urease method;the serum content of interleukin cells 6 (IL-6) and tumor necrosis factor(TNF-α) was measured byeuzymelinked immunosorbent assay;uate transporter 1 (URAT1) and glucose transporter 9 (GLUT9) in mouse kidneys were measured by quantitative fluorescence analysis.Kidney tissues were harvested and histopathological changes were observed by HE staining.Results Compared with the normal group,the UP, UUN, UA, BUN, IL,URAT1 and ULUT9 of model group mice were significant increased (P<0.01),TNF-α was increased (P<0.05),the renal tissue structure was normal.Compared with the model group,the UP,UUN,UA,BUN of benbromarone positive drug group were significant decreased(P<0.01),IL-6 and TNF-α were decreased(P<0.05),URAT1 was increased(P<0.05),little glomerular atrophy and deformation in the kidney,kidney tubular dilatation was occasionally seen,and no inflammatory cell infiltration.Compared with the model group,the UP,UUN,UA,BUN,IL-6 and URAT1 of high-dose group of compound active tea of Lithocarpus litseifolius were significant decreased(P<0.01),TNF-α and GLUT9 levels were decreased(P <0.05);the UP, UA, UUN content , the levels of IL-6, URAT 1and GLUT9 of middle-dose group of compound active tea of Lithocarpus litseifolius were significant decreased(P<0.01),BUN together with reduced levels of TNF-α(P <0.05);the UP,UUN,UA,IL-6 and URAT1 of low-dose group of compound active tea of Lithocarpus litseifoliuswere significant decreased(P<0.01),BUN content and reduction of TNF-α and GLUT9 levels (P<0.05),the kidney condition of the mice in compound active tea of Lithocarpus litseifolius group was improved.Conclusion: the compound active tea of Lithocarpus litseifolius can reduce uric acid in mice with hyperuricemia nephropathy, and it has a certain protective effect on the kidney,the mechanism may be related to the inhibition of uric acid reabsorption, and the specific mechanism should be further investigated.
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HDAC6 inhibitors improve diabetic nephropathy by protecting glomerular endothelial cell mitochondria

ChenXiaoli

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objective: To investigate the protective effect and mechanism of histone deacetylase 6 (HDAC6) specific small molecule inhibitor Tubastatin A on renal injury in diabetic nephropathy (DN) mice. Methods: C57BL/6 mice were randomly divided into 3 groups: control group, DN group and Tubastatin A group. Mice in the DN group and Tubastatin A group were intraperitoneally injected with燬TZ?80爉g/kg) daily for 3 days after the removal of one kidney. Tubastatin A group received Tubastatin A treatment every 3 days for 8 weeks. RNA sequencing analysis of differentially expressed genes in kidney tissue of DN group and Tubastatin A group. Mitochondrial damage was assessed by transmission electron microscopy, and ROS levels in kidney tissue were estimated by DHE staining. Mouse glomerular endothelial cells (mGEC) were exposed to high glucose medium (HG) or 40 mM mannitol (control) with or without Tubastatin A treatment. Western blot analysis was used to analyze the expression of HDAC6, kidney injury markers KIM1 and EMT markers, and flow cytometry was used to detect mitochondrial ROS and apoptosis in cells. Results: HDAC6 expression was up-regulated in DN mouse kidney tissue and mGEC cells exposed to HG, consistent with increased levels of KIM1. Histological analysis showed significant morphological changes in DN mice, including glomerular hypertrophy, mesangial matrix accumulation, glomerular basement membrane thickening, tubular basement membrane thickening and the presence of glomerular, intertubular fibrosis; Tubastatin A treatment alleviated these changes. Compared with control DMSO, Tubastatin A significantly decreased the expression of KIM1, HDAC6, α-SMA, N-cadherin, vimentin (P<0.05) and up-regulated the expression of E-cadherin (P<0.05) in mGEC cells under HG treatment. RNA-sequencing revealed the enrichment of genes related to ECM-receptor interaction and tricarboxylic acid (TCA) cycle in the kidney tissue of Tubastatin A mice compared with DN mice. Transmission electron microscopy showed that the proportion of damaged mitochondria in glomerular endothelial cells in Tubastatin A group was significantly lower than that in DN group (P<0.01). DHE staining showed that the level of ROS in the kidney tissue of Tubastatin A group was lower than that of DN group (P<0.01). In mGEC cells, Tubastatin A treatment down-regulated HG-induced mitochondrial ROS levels in mGEC cells (P<0.01), and reduced apoptosis (P<0.05). Conclusion: Tubastatin A ameliorates HG-induced glomerular endothelial cell injury and DN progression, and its mechanism is related to the protection of mitochondrial homeostasis and inhibition of EMT.
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Effects of human amniotic epithelial cells transplantation on the improvement of endometrium and MMP-8, VEGF in rat model of uterine scar

王静

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Objective: To investigate the effect of human amniotic epithelial cells (hAECs) transplantation on endometrium improvement and matrix metalloproteinase-8 (MMP-8) and vascular endothelial growth factor (VEGF) in a rat model of uterine scar. Methods: The uterine scar model of rats was established and randomly divided into model group and transplantation group, with 18 rats in each group. The other 18 rats were selected as sham operation group. The rats in the transplantation group were injected with hAECs in the scar of the uterus, and the rats in the model group and the sham operation group were only given the same amount of PBS. After 4 weeks, the uterine tissues of 8 rats in each group were collected and HE staining was used to observe the histomorphological changes, and the endometrial thickness and the number of glands were measured. Masson staining was used to observe endometrial fibrosis. Endometrial growth and receptivity were evaluated by immunohistochemical staining for cytokeratin and integrin β3, respectively. The mRNA expression levels of MMP-8 and VEGFA in endometrial tissues were detected by RT-qPCR. Western blotting was used to detect the protein expression levels of MMP-8 and VEGFA. After 8 weeks, the remaining 10 rats in each group were selected for gestational ability determination. Results: Compared with the sham-operation group, the endometrial thickness, the number of glands, the IOD value of keratin and integrin β3, the mRNA and protein relative expression levels of MMP-8 and VEGFA, the pregnancy rate and the number of uterine embryos in the model group and the transplantation group were significantly decreased (P<0.05). Compared with the model group, the endometrial thickness, the number of glands, the IOD value of keratin and integrin β3, the mRNA and protein relative expression levels of MMP-8 and VEGFA, the pregnancy rate and the number of uterine embryos were significantly increased in the transplantation group (P<0.05). In addition, hAECs transplantation could improve the pathological morphology of endometrial tissue in rats with uterine scar. Reduce the degree of endometrial fibrosis. Conclusion: hAECs transplantation could improve endometrial injury, reduce scar formation, improve endometrial receptivity, and enhance pregnancy function in model rats, which may be related to the promotion of MMP-8 and VEGFA expression.
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Effect of inhibition of the mitochondrial inner membrane protein OMA1 on apoptosis in a Rot-induced Parkinson's disease cell model

shijin, Lihaining, Luyue, Xuting

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Objective To investigate the effect of inhibition the mitochondrial inner membrane protein OMA1 on rotenone-induced apoptosis in Parkinson's disease (PD) cell model. Methods SH-SY5Y cells were cultured in vitro, treated with Rot (final concentrations of 0.05, 0.1, 0.2, 0.3, 0.4 μmol/L) for 24 h, and the best Rot (0.2 μmol/L) was selected for subsequent experiments. The experiment was divided into control group (cells without special treatment), PD model group (0.2 μmol/L Rot treated cells for 24 h), Negative control group (negative control sequence of OMA1 siRNA transfected on the basis of normal control group), OMA1 siRNA group (0.2 μmol/L Rot treated cells for 24 h and transfected with OMA1 siRNA). CCK-8 was used to detect cell survival rate, inverted phase contrast microscope was used to observe cell morphology in each group, Western blot was used to detect changes in the expression of OMA1 and apoptosis-related proteins Caspase-3, Bax, and Bcl-2, and TUNEL apoptosis kit was used to detect cell apoptosis. Results Compared with the control group, the survival rate of SH-SY5Y cells decreased in a concentration-dependent manner with increasing Rot concentration (P<0.05). Compared with the control group, the expression of OMA1 and apoptotic protein Caspase-3 expression were increased and Bax/Bcl-2 values were increased in the PD model group (P<0.01). Compared with the PD model group, the cells in the OMA1 siRNA group, the OMA1 siRNA group gradually restored morphological changes, decreased apoptotic protein Caspase-3 expression and Bax/Bcl-2 values, and TUNEL apoptosis staining suggested reduced apoptosis (P<0.01). Conclusions Inhibition of the mitochondrial inner membrane protein OMA1 ameliorates apoptosis induced by the Rot-induced PD cell model, which in turn may have a protective effect on neurons.
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The effect of CeO2NPs on organ structures and redox indicators in male mice

yin jun

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Objective To investigate the effects of CeO2NPs sub-acute exposure on body weight, organ structures and redox indicators in male mice. Methods 35 male ICR mice were randomly divided into five groups with seven mice in each group. Normal control group and CeO2NPs (100, 500, 1000, 5000 ug/kg) test groups were set up. Mice were injected CeO2NPs intraperitoneally every other day for 28 days. Results Compared with the control group, there was no significant difference in weight gain (P>0.05) , but there was significant difference in liver coefficient, epididymal coefficient and sperm survival rate (P<0.01). In the 5000 ug/kg group, CeO2NPs were deposited in the liver and spleen, and granuloma was found. The activities of SOD and GSH-Px in serum of 100 ug/kg group were increased, while the content of MDA was decreased, which showed the antioxidant effect of CeO2NPs. With the increase of dose, the oxidative stress induced by CeO2NPs was enhanced. Conclusion The low dose of CeO2NPs is safe and has antioxidant effect. With the increase of dose, the toxicity of CeO2NPs to the body also increases gradually.
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Research progress on gut microbiota and obesity-related metabolic diseases

Su Hei Yan Pa Er Ha Ti, ZHANG Jiaojiao, MA Zhuang, WANG Junren, LI Yanhong

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Obesity centered metabolic diseases such as diabetes, hypertension, and cancer are increasing at an alarming rate worldwide and have become global public health concerns. The treatment of obesity and related metabolic diseases has gradually become a research hotspot. Currently, an increasing number of studies have proved that gut microbiota can regulate energy balance and glycolipid metabolism, and regulate the occurrence and development of obesity and related metabolic diseases. It is very likely that the gut microbiota is a potential new target for the treatment and prevention of metabolic diseases. In this paper, we summarize the progress of gut microbiota in the development and progression of obesity associated metabolic diseases and analyze the role of gut microbiota in metabolic diseases.
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Research progress of exosomal microRNA in early screening and treatment of Alzheimer's disease

zhangjunfeng

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Exosomes, as small molecule extracellular vesicles secreted by a variety of cells, play an important role in the pathological process of Alzheimer's disease by transporting a variety of bioactive substances such as microRNA. Studies have shown that the expression of exosomal microRNA changes in the early stages of AD patients, and exogenous injection of mesenchymal stem cell-derived exosomal microRNA can improve the learning and memory ability of AD animal models. This paper reviews the research progross of exosomes in early screening and treatment of Alzheimer's disease.
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Research progress of disease-syndrome combination models of chronic obstructive pulmonary disease

badeting, HAO Binbin, LI Juan

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Chronic obstructive pulmonary disease (COPD) is a common respiratory disease with high morbidity and mortality, which has become an important health problem in today's society. Traditionray Chinese Medicine has accumulated rich historical experience in the treatment of COPD and has unique clinical advantages. In order to further explore the therapeutic effect of traditional Chinese medicine on this disease, the preparation of COPD animal model combining disease and syndrome is the key premise of studying the occurrence and development of the disease. The combined models of disease and syndrome summarized in this paper include five types: the animal model of lung qi deficiency, the animal model of lung and spleen deficiency, the animal model of phlegm-heat stagnation of lung, the animal model of phlegm-stasis obstructing lung, and the animal model of cold drink. Now the common disease and syndrome in recent years combined with the method of class modeling are simply described and combed, in order to provide new ideas for researchers, and promote the research process of traditional Chinese medicine treatment of this disease.
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Research Progresses on the Effects of the Plateau on Mitochondrial Function and Energy Metabolism

LIBOSHEN, ZHANGYUXUAN, FANRONGHUI, LIMAOXING

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The plateau is a unique environment with low pressure, low oxygen and high cold. The plateau environment will reduce the metabolism of energy substances and mitochondrial work, thus affecting the plateau operation. In recent years, mitochondrial damage has attracted wide attention. As the energy factory of cells, mitochondria are closely linked to the movement of the body. We focused our attention on mitochondrial damage at high altitude, and summarized the effects of high altitude on the metabolism of basic energy substances and the changes of key enzyme activities and mitochondrial structure and function in mitochondrial biochemical energy supply response. It was found that protein, carbohydrate and lipid metabolism was negatively affected at high altitude, resulting in fatigue, hyperlipidemia and body repair. The activities of enzymes related to pyruvate metabolism, tricarboxylic acid cycle, β-oxidation and oxidative phosphorylation are inhibited, and the morphology and number of mitochondria are changed, which will lead to impaired mitochondrial function and affect exercise energy supply. In the future, the exploration of the mechanism of plateau cell injury will vigorously promote the research of plateau injury prevention and treatment drugs.
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A review of animal models of vascular dementia

songyuanyu, chenyinghua

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Abstract: Vascular Dementia (VD) is caused by cerebrovascular diseases, either hemorrhage or ischemic damage in the brain, with ischemia being the most common. In recent years, much more efforts have been made to study the etiology, pathogenesis and prevention of VD. The establishment of appropriate animal models for studying the mechanism of VD and exploring efficacy of VD treatment has become one of key issues in the research field. On the basis of the conventional methods such as the bilateral occlusion of the common carotid arteries (2VO) and the four-vessel occlusion, the researchers had modified these methods to improve the stability with better reflection of the clinical manifestations of VD. This paper mainly summaries these modified methods, and discuss possible cellular and molecular mechanisms and their advantages and disadvantages.
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Keratin 17 knockout aggravates wound healing in diabetic mice

Bao Dan, Guo Rui, Hou Daorong

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Objective To explore the effects of keratin 17 (Krt17) knockout on wound healing in diabetic mice. Methods To establish the diabetic models, 60% high-fat diet was fed and streptozotocin was administered intraperitoneally at 40mg/kg once per day for 5 consecutive days in wild-type (WT) and Krt17 knockout (Krt17-/-) mice at six weeks of age. The mice were anesthetized with isoflurane, the back was shaved, and a 6 mm circular skin lesion was made in vivo at one week after successful modeling. Western blotting and immunofluorescence staining were used to detect the expression and localization of KRT17 and histopathological examination was analyzed in wound healing on the 8th day. Photos were taken at 0, 2, 4, 6 and 8 days after wound manufacturing, and wound healing rate was calculated. Results KRT17 was mainly expressed in mouse hair follicles in physiological conditions. When the skin was injured, the expression of KRT17 in keratinocytes in the proximal wound was significantly increased. However, the expression of KRT17 in wounds of diabetic mice was significantly down-regulated compared with that of control mice. The wound healing rate of Krt17-/- mice was significantly reduced and the local inflammatory reaction was more persistent compared with WT mice. Conclusions Krt17 knockout aggravates wound healing in diabetic mice. Krt17 may be an important modifier gene of diabetic wound healing.
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Effects of baicalin on proliferation and apoptosis of laryngeal cancer cells via miR-125b-5p/IRF4 axis

WANGJIAN, SUNYONGDONG, ZHOUXINGWEI, LIULEI, TONGXINGKE, CHENLONG, HEXIAN

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Objective: To explore the mechanism of baicalein inhibiting the proliferation and migration of laryngeal cancer cells. Methods: Hep-2 cells were used as the research object. The cell proliferation activity of each group was detected by MTT method, cell migration was detected by scratch assay, cell apoptosis was detected by flow cytometry, western blot was used to detect the expression levels of Beclin-1, LC3II/I, p62 and HDAC1 in laryngeal cancer cells in each group, RT-PCR detection of the expression levels of miR-449a in each group of cells. The targeted binding sites of miR-449a and HDAC1 were analyzed by bioinformatics software and identified by dual luciferase reporter gene experiments. The number of autophagosomes was observed by projection microscopy. Results: Baicalein significantly inhibited the proliferation and migration of laryngeal cancer cells, and significantly induced apoptosis. Baicalein increased the protein expression levels of intracellular autophagy-related genes Beclin1 and LC3II, but decreased the protein expression levels of p62 and LC3I. Baicalein significantly increased the expression level of miR-449a in laryngeal cancer cells and decreased the protein expression of HDAC1. There is a binding effect between HDAC1 and miR-449a. Baicalein combined with miR-449a mimic to treat laryngeal cancer cells can more significantly inhibit cell proliferation and HDAC1 protein expression, as well as more effectively up-regulate the relative expression of miR-449a and induce autophagy. Conclusion: Baicalein can mediate autophagy and inhibit the proliferation and migration of laryngeal cancer cells via the miR449a/HDAC1 axis.
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Effects of low-dose BPA and DEHP on the expression of AKR1C3 in prostate of adult rats

Huangdongyan, Wushuangshuang, Shaocongcong, Suxin, Yangrongfu, Wangkaiyue, Zhouping, Wujianhui

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Objective To investigate the effects of of low dose of bisphenol A (BPA) and di (2-ethyl) hexyl phthalate (DEHP) on Aldo-keto reductase 1C3 (AKR1C3) in adult SD rats. Method 56 adult male SD rats were randomly divided into 7groups (8 rats in each group) and they were given BPA (10.0µg/kg,30.0µg/kg,90µg/kg, i.g.), DEHP (30.0µg/kg ,90.0µg/kg ,270 µg/kg, i.g.) and vehicle respectively once a day for 4 weeks. The animals were sacrificed on the day subsequent to last treatment and the blood was collected, the prostate tissues were dissected and categorized into different lobes. The levels of AKR1C3 in serum and prostate were detected by enzyme-linked immunosorbent assay (ELISA), and the expression of AKR1C3 in each lobe of prostate was analyzed by immunohistochemistry. Result After the administration of BPA, the expression of AKR1C3 in 90µg/kg and 270µg/kg group increased, and there was significant difference in the high-dose group (P<0.05); The level and protein expression of AKR1C3 in dorsal prostate increased, and there was significant difference in 10µg/kg group (P<0.01, P<0.001). After administration of DEHP, the level of serum AKR1C3 in 270µg/kg group was significantly higher than that in the control group (P<0.001), the level of AKR1C3 in the ventral prostate was significantly higher than that in the control group (P<0.05, P<0.01), and the expression of AKR1C3 protein increased, there was significant difference in 270µg/kg group (P<0.05); The level of AKR1C3 in 90µg/kg and 270µg/kg dose group of dorsal prostate was higher than that in the control group, and there was significant difference in 30µg/kg group (P<0.05). The expression of AKR1C3 protein in each group increased, and there was significant difference in 30µg/kg and 90µg/kg dose group (P<0.001, P<0.05). Conclusion Low-dose BPA and DEHP can promote the expression of AKR1C3 in the prostate of adult SD rats, but the sensitivity of ventral and dorsal lobes of prostate to BPA and DEHP is different.
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Bone marrow mesenchymal stem cells isolated from rats by bone marrow and slice adherent culture in vitro and PKH26 labeling

Chen Shuang, Yan Zhenyu

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Objective To establish an efficient method for isolation and culture of rat bone marrow mesenchymal stem cells (BMSCs), and apply PKH26 to label them in vitro to explore the effect of PKH26 labeling on the biological characteristics of BMSCs, as well as the in vitro tracing. Methods The bone of both hind limbs of 5d suckling rats were separated, the surrounding muscle and fascia were removed, and cut into small pieces for culture. BMSCs were purified by fluid exchange and passage, and the third generation cell surface antigen was determined by flow cytometry. Under the same culture conditions, the third generation BMSCs were labeled with PKH26. Cell morphology and proliferation status were observed under fluorescence microscope in the labeled group and the unlabeled group, and the adipogenic induction characteristics and identification of the labeled group and the unlabeled group were compared. Results The bone marrow slice method was used to separate the hind limb bones of suckling mice. The BMSCs were slender spindle shaped and uniform in shape. A large number of BMSCs could be rapidly obtained in a short time; The results of flow cytometry showed that the expression of CD29 was (91.18 ± 1.29)%, the expression of CD90 was (91.18 ± 1.29)%, and the expression of CD45 was (1.74 ± 0.36)%; PHK26 labeling had no significant effect on the morphology and proliferation of BMSCs cells (P>0.05), and had no effect on the induction of osteogenesis and adipogenesis. Conclusions A large number of high-purity BMSCs can be rapidly cultured by the method of 5-day rat bone marrow slices, which can be used as seed cells for bone tissue engineering; PKH26 can label rat BMSCs in vitro.
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Regulation of ADAM10 gene osteogenic differentiation of bone marrow mesenchymal stem cells and tibial fracture union through Notch1 pathway

TangXiaoxu, Liu wanting, Douyinxia, Li Fuqin, Wang Nan

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Objective To study the regulation of a disintegrin and metalloproteinase 10 (ADAM10) gene on osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and tibial fracture union. Methods BMSCs of SD rats were cultured, BMSCs stably transfected with negative control (NC) shRNA or ADAM10 shRNA pGFP-V-RS vector were established, the osteogenesis was induced for 14 days. During the induction process, DMSO or 10 μmol/L Notch1 agonist valproic acid (VPA) were added. absorbance at 405nm of alizarin red staining, ALP activity and the expression levels of ADAM10, OCN, Runx2, CoL-I, NICD and Hes1 were detected. The tibial fracture model of SD rats was established and NC shRNA or ADAM10 shRNA pCMV5.0 vector was injected locally. The fracture healing and gene expression were observed for 4 weeks later. Results The expression level of ADAM10 in BMSCs in sh-ADAM10 group was lower than that in sh-NC group. After osteogenesis induction, the absorbance value of alizarin red staining at 405nm, ALP activity and the expression levels of OCN, Runx2, CoL-I, NICD and Hes1 of sh-ADAM10 group were higher than those in sh-NC group (P<0.05). the absorbance value of alizarin red staining at 405nm, ALP activity and the expression levels of OCN, Runx2, CoL-I of sh-ADAM10 VPA group after osteogenesis induction were lower than those in sh-ADAM DMSO group (P < 0.05). The fracture healing of tibial fracture rats in sh-ADAM10 group was better than that in sh-NC group, and the expression levels of OCN, Runx2, CoL-I, NICD and Hes1 were higher than those in sh-NC group (P<0.05). Conclusion Knockdown of ADAM10 can promote the osteogenic differentiation of BMSCs and the healing of tibial fractures by inhibiting Notch1 pathway.
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The improvement effect and mechanism of modified Chaihu Guizhi Decoction on osteoporosis rats by regulating Wnt/β-catenin signaling pathway

Guo Zhonghua, Cao Yuju

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Objective: To investigate the improvement effect of modified Chaihu Guizhi Decoction (CGD) on osteoporosis rats by regulating the Wnt/β-catenin signaling pathway. Methods: SD rats were separated into CK group, Model group, low-dose CGD group (CGD-L group, 5 g/kg), high-dose CGD group (CGD-H group, 20 g/kg), and estradiol valerate group (EV group, 9 mg/kg), DKK-1 (Wnt/β-catenin pathway inhibitor) group (100 mg/kg), and CGD-H DKK-1 group (20 g/kg 100 mg/kg), 12 per group. Except for the CK group, the rats in other groups were given 70 mg/kg retinoic acid to build the OP rat model, and the rats in the CK group were given the same amount of normal saline. From the 4th week of modeling, the corresponding drug intervention was given for 4 weeks. ELISA was applied to detect the levels of collagen type I C-terminal peptide (CTX-Ⅰ) and osteocalcin (BGP) in serum of rats; the changes of bone volume fraction, bone trabecular thickness, bone mineral density and bone trabecular number were observed; HE staining was applied to detect the pathological changes of rat femur; Alkaline phosphatase (ALP) calcium-cobalt staining was applied to detect osteoblast activity in rat femur; the activity of osteoclasts in rat femur tissue was detected by tartrate-resistant acid phosphatase (TRAP) staining; Western blot was applied to detect Wnt and β-catenin proteins in femoral tissue of rats in each group. Results: Compared with the CK group, the femoral tissue of the Model group had severe pathological damage, CTX-I level and osteoclast activity increased, BGP level, bone volume fraction, bone trabecular thickness, bone mineral density, bone trabecular number, osteoblast activity, Wnt, β-catenin protein expression decreased (P<0.05); compared with the Model group, the pathological damage of the femur in the CGD-L group, the CGD-H group and the EV group was alleviated, CTX-I level and osteoclast activity decreased, BGP level, bone volume fraction, trabecular thickness, bone mineral density, bone trabecular number, osteoblast activity, Wnt, β-catenin protein expression increased, the trends of the corresponding indicators in the DKK-1 group were opposite to the above (P<0.05); compared with the CGD-H group, the femoral tissue of the CGD-H DKK-1 group was severely damaged, CTX-I level and osteoclast activity increased, BGP level, bone volume fraction, bone trabecular thickness, bone mineral density, bone trabecular number, osteoblast activity, Wnt, β-catenin protein expression decreased (P<0.05). Conclusion: CGD may improve OP of rats by activating the Wnt/β-Catenin pathway.
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Acupoint catgut embedding affects the level of inflammation in rheumatoid arthritis through PD-1/OX40 signaling pathway

Chen Li-chuan, Duan bo, Yu Zhao, Ma Zhi-yi, Meng Qian-wen

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Objective: This experiment studied the effect and mechanism of acupoint catgut embedding on rheumatoid arthritis by regulating PD-1 / OX40 signal pathway. Methods: 25 female SD rats were induced with complete Freund's adjuvant to establish rheumatoid arthritis model rats, and then treated with acupoint catgut embedding and drug therapy. The rats were divided into 5 groups: control group, model group, leflunomide group, acupoint catgut embedding group and acupoint catgut embedding leflunomide group. The degree of inflammation was judged by evaluating the arthritis index; The contents of serum IL-6 and IL-8 were detected by ELISA; He staining was used to observe synovitis cell infiltration, smooth abdominal tissue, fibrous tissue, macrophage proliferation and angiogenesis; The contents of PD-1 / OX40 and CD4 cd28-pd-1lowox40 T cell subsets were detected by flow cytometry. Results: except the control group, there were erythema and moderate swelling from ankle to metatarsal or metacarpal joint in each group. After 14 days, there was no significant change in the score of the model group, but the inflammatory factor scores of leflunomide group, acupoint catgut embedding group and acupoint catgut embedding leflunomide group began to decline, and the acupoint catgut embedding leflunomide group decreased the fastest. The contents of IL-6 and IL-8 in serum of model group increased significantly (P < 0.01), and the contents of IL-6 and IL-8 in serum of rats in flutamide group, acupoint catgut embedding group and acupoint catgut embedding leflunomide group decreased significantly (P < 0.01). The synovial tissue of the model group was damaged, with a large number of inflammatory cell infiltration, vascular dilatation and fibroblast proliferation. After leflunomide and acupoint catgut embedding treatment, the inflammatory cell infiltration in the synovial tissue of the model group was significantly reduced and the vascular proliferation was inhibited, and the effect was the most obvious when Leflunomide and acupoint catgut embedding worked together. In the model group, the content of pd-1lowox40 decreased significantly (P < 0.01), the content of CD4 cd28-pd-1lowox40 T cells increased significantly (P < 0.01), and the content of pd-1lowox40 in acupoint catgut embedding group and leflunomide acupoint catgut embedding group increased significantly (P < 0.01) The content of CD4 cd28-pd-1lowox40 T cells in acupoint catgut embedding group and acupoint catgut embedding leflunomide group decreased significantly (P < 0.01). Conclusion: acupoint catgut embedding can improve the symptoms of rheumatoid arthritis, and has the effect of combined treatment with leflunomide. Its mechanism may be related to PD-1 / OX40 signal pathway.
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Left to right shunt slows cardiac remodeling in rats with pulmonary hypertension

jishuang

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【Abstract】Objective: The prognosis of patients with left-to-right shunt congenital heart disease associated pulmonary hypertension is significantly better than that of idiopathic pulmonary hypertension, but the specific mechanism is unclear. The purpose of this project is to make a rat model of idiopathic pulmonary hypertension and congenital heart disease with pulmonary hypertension, and compare the similarities and differences between the two models in pulmonary vascular remodeling and cardiac remodeling. Methods: Male SD rats were divided into three groups: control group (n=8), monocrotaline (MCT) group (50mg/kg) to simulate idiopathic pulmonary hypertension (n=8); Cervical arteriovenous shunt surgery monocrotaline (MCT) group (50mg/kg) simulated left to right shunt congenital heart disease with pulmonary hypertension (n=8). Three weeks after the establishment of the model, echocardiography, left and right cardiac catheter pressure measurement and lung histopathological staining were performed to compare the cardiac and pulmonary phenotypes of the rats. Results: Compared with the control group, there was no significant difference between the MCT group and the operation MCT group in the right ventricular hypertrophy, right ventricular dysfunction, mean pulmonary artery pressure, pulmonary vascular remodeling and other indicators 3 weeks after operation. But in many indexes related to left heart, the rats in the operation MCT group were significantly better than those in the simple MCT group. Compared with the control group, the left ventricular lumen diameter (LVID; d) and left ventricular ejection fraction (EF%) in the operation MCT group did not decrease in the diastolic period; The maximum rate of increase of right ventricular internal pressure (MAX dp/dt) and the maximum rate of decrease of left ventricular internal pressure (MIN dp/dt) in the operation MCT group were lower than those in the simple MCT group. Conclusion: Left to right shunt surgery can not change MCT-induced pulmonary hypertension and right heart remodeling, but can produce left heart compensation, which may be beneficial to the prognosis of patients. The animal model of this project establishes the basis for studying the different pathological mechanisms of idiopathic pulmonary hypertension and pulmonary hypertension associated with congenital heart disease.
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Monkeypox virus infection and the animal model of Monkeypox

bao rong

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Monkeypox is an infectious disease caused by Monkeypox virus （MPXV） infection. The host of MPXV remains unclear, and rodents and nonhuman primates consider the potential hosts. Monkeypox is rapidly spreading globally. However, the animal models for Monkeypox have not developed in the last decades in China. MPXV is a pathogen that seriously threat to human health. Its transmission among the population has presented new characteristics. Therefore, this article describes the discovery of MPXV and the early epidemic, different types of infection and co-infection. In addition, the experimental infection and animal models for Monkeypox in rodents and nonhuman primates were expounded in this paper.
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The expression of IGHG1 in acute myeloid leukemia THP-1 cell and the influences on cell proliferation, apoptosis and invasion by regulating TGF-β/Smad pathway

Lichangmei, Qiuli

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Objective To investigate the expression of immunoglobulin γ-1 heavy chain constant region (IGHG1) in acute myeloid leukemia (AML) THP-1 cell and its influences on cell proliferation, apoptosis and invasion by regulating the transforming growth factor β (TGF-β)/Smad pathway. Methods The bone marrow specimens of 9 children with AML, the bone marrow specimens of 8 children with fracture,human bone marrow stromal cells HS-5 and human AML cells THP-1, HL60 were used as research objects,Western Blot was used to detect IGHG1 protein expression; THP-1 cells were divided into: blank group (cells without any treatment), si-NC group, si-IGHG1-1 group, si-IGHG1-2 group, si-IGHG1-3 group, TGF-β group,si-IGHG1-1 TGF-β group,si-IGHG1-1 TGF-β LY364947 group, CCK-8 method was used to detect cell proliferation; apoptosis was detected by flow cytometry; Transwell experiment was used to detect cell invasion ; Western blot was used to detect the protein expression of IGHG1, TGF-β, p-Smad2, and p-Smad3 in each group of cells. Results Compared with the bone marrow of children with fracture, the expression level of IGHG1 protein [(0.24?.03) vs (0.87?.12] in the bone marrow of children with AML was significantly higher (P<0.05); compared with HS-5 cell, the expression level of IGHG1 protein in human AML cells THP-1, HL60 was significantly increased [(0.89?.14)(0.75?.08) vs (0.21?.02)] (P<0.05); compared with the blank group , the OD450 value (24, 48, 72h) of THP-1 cells, the number of invaded cells, and the protein expression of TGF-β, p-Smad2, and p-Smad3 were significantly reduced in the si-IGHG1-1 group, and the apoptosis rate was increased (P<0.05), while the corresponding indexes in TGF-β group were opposite (P<0.05); the TGF-β reversed the effects of silencing IGHG1 on the proliferation, apoptosis and invasion of THP-1 cells; compared with si-IGHG1-1 TGF-β group, TGF-β, p-Smad2, p-Smad3 protein, OD450 values (24, 48, 72 h) and invasion number of cells decreased significantly in si-IGHG1-1 TGF-β LY364947 group, and the cell apoptosis rate was increased (P<0.05). Conclusions IGHG1 is highly expressed in AML cells. Silencing IGHG1 can inhibit the proliferation and invasion of AML cells, and promote the apoptosis of AML cells. This mechanism may be related to the inhibition of TGF-β/Smad pathway.
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The relationship between atmospheric pollutants and some adverse pregnancy outcomes

jinjian, Chang Hui, Huang Hehuan, Peng Rui, Zhang Xiaoan

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With the rapid development of China's economy and the continuous acceleration of urbanization, the problem of air pollution is becoming increasingly prominent, which has a great impact on human health. In recent years, a large number of research work has emerged both domestically and internationally, and research results have shown a certain correlation between exposure to atmospheric pollutants during pregnancy and adverse pregnancy outcomes. The impact of air pollution on the health and embryonic development of pregnant women has received more attention. This article mainly provides a brief review on the impact of atmospheric pollutants on some adverse pregnancy outcomes and their possible biological mechanisms.
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Research Progress on Model Organism Zebrafish in Neurodegenerative Diseases

Huang Kongli, Su Shijie, Wang Yuting, LIU ZHUANGZHUANG, CAO DANDAN, WANG PEI, CHEN GUANLIN, Wang Qi

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Neurodegenerative disease （NDD）is a chronic and progressive neurological disease characterized by the loss of a large number of specific neurons. It mainly includes Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD) and amyotrophic lateral sclerosis (ALS). Although the lesions and etiologies of different types of neurodegenerative diseases are different, delayed neurodegenerative lesions and cell loss in specific brain areas are their common characteristics. For this reason, it is collectively referred to as neurodegenerative diseases. In recent years, zebrafish have attracted increasing attention from society as a new type of model organism. Although there are some differences between zebrafish and human central nervous systems, zebrafish neural conduction systems, neuronal and glial cell types, and disease-related gene homology are very similar to those of humans. Zebrafish has been widely used in the study of neurodegenerative diseases, and some achievements have been made in this field to improve our understanding of these diseases, but because of the complexity, multi-factors and multi-gene regulation of neurodegenerative diseases, the etiology and pathogenesis of zebrafish are not clear, so the treatment of this kind of disease has always been a difficult problem. By consulting relevant literature from home and abroad in recent years, this study reviews recent advances in neurodegenerative diseases using zebrafish as a model organism.
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Progress in irisin and its upstream and downstream antidepressants

Sangjiala, Lishanshan, Cuixin, Renqingqing, Houruiling, Panxingfang, Wangshenjun, Zhao

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Depression is the main cause of disability, and the adverse effects on people are difficult to eliminate. Despite the increasing number of antidepressants, depression is still not adequately treated clinically, and new mechanisms still need to be explored. As the beneficial effects of irisin on the nervous system are gradually elucidated, studies have found that irisin has an antidepressant effect, and irisin may become a new target for the treatment of depression. This study aims to explore the mechanism of irisin and its upstream and downstream antidepressants, by reviewing the existing studies to explain the link between depression and irisin, propose the potential mechanism of SIRT1 / PGC-1α mediating FNDC5/Irisin to regulate BDNF and promote neurogenesis to improve depression, and provide a new idea for the study of irisin and its upstream and downstream antidepressants.
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Advances of CREB in the regulation of memory through synaptic plasticity and its relation with Alzheimer’s disease

Luo Zhuohui, pang shuo, Zhang lianfeng

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Alzheimer’s disease is an irreversible heterogeneous neurodegenerative disease. AD patients are featured with memory loss and impaired synaptic plasticity. With a view to cAMP responsive element-binding protein which is intimately associated with synaptic plasticity. this assay summarized progress on the structure, signal pathway, downstream genes and relative memory regulation. The involvement of CREB in AD development would serve as references for AD researches based on synaptic plasticity improvement.
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Research progress on the regulation of lymphangiogenesis and its role in myocardial infarction

duqing, wanghe

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Lymphatic system plays an important role in regulating interstitial fluid homeostasis, lipid metabolism and immune function. After myocardial infarction, enhanced lymphangiogenesis accelerates the clearance of infiltrating immune cells, reduces the production of pro-inflammatory cytokines, reduces edema, inflammation, and fibrosis, and promotes the recovery of damaged heart function. Vascular endothelial growth factor-C (VEGF-C) and its receptor VEGFR-3 are components of the lymphangiogenesis pathway and play a critical role in maintaining tissue fluid balance and myocardial function after cardiac injury. Lymphatic vessels are closely related to the immune system. Different immune cell groups can stimulate or inhibit lymphatic remodeling. Macrophages are congenital immune cells widely distributed in organs and tissues, and play an important role in various physiological and pathological processes such as organ development, host defense, acute and chronic inflammation, tissue homeostasis and remodeling. More mechanisms of lymphangiogenesis need to be identified to provide effective targets for clinical stimulation of lymphangiogenesis to treat heart disease. This paper reviews the basic pathological changes of the heart and lymphatic vessels after myocardial infarction, the regulatory factors of lymphangiogenesis, and the influence of macrophages on lymphangiogenesis.
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Effects of LncRNA FGD5-AS1 targeting and regulating miR-129-5p on the proliferation, apoptosis, migration and invasion of oral squamous cell carcinoma cells

Yangfeng, Liuguanglong

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Objective To investigate the effects of long non-coding RNA (LncRNA) FGD5-AS1 on the proliferation, apoptosis, migration and invasion of oral squamous cell carcinoma (OSCC) cells through targeted regulation of miR-129-5p. Methods The expression of FGD5-AS1 in OSCC was analyzed by online database. The tumor tissues, normal tissues, and the human oral mucosal cells (HOK) and OSCC cells (SCC-9, HSC-4, SCC-25, CAL-27) cultured in vitro from 30 OSCC patients collected in our hospital were used as research subjects, qRT-PCR method was performed to detect the expression of FGD5-AS1 and miR-129-5p. The CAL-27 cell line with the highest FGD5-AS1 expression was randomly separated into Control group (normal culture, no transfection), si-NC group (transfected with si-NC), si-FGD5-AS1 group (transfected with si-FGD5-AS1), si-FGD5-AS1 NC inhibitor group (co-transfected with si-FGD5-AS1 and NC inhibitor) and si-FGD5-AS1 miR-129-5p inhibitor group (co-transfected with si-FGD5-AS1 and miR -129-5p inhibitor), CCK-8 method and clone formation assay were used to detect the proliferation ability of CAL-27 cells; the apoptosis level of CAL-27 cells was detected by flow cytometry; the migration ability of CAL-27 cells was detected by wound-healing assay; Transwell chamber was used to detect the invasion ability of CAL-27 cells; and dual luciferase reporter experiment verified the targeting relationship between FGD5-AS1 and miR-129-5p; the expression of high mobility group protein B1(HMGB1) was detected by Western blot. In vivo xenograft tumor model was constructed and divided into sh-NC group, sh-FGD5-AS1 group, miR-129-5p inhibitor group, and sh-FGD5-AS1 miR-129-5p inhibitor group. Tumor volume and tumor were detected. QRT-pcr was used to detect the expression of FGD5-AS1 and miR-129-5p in transplanted tumor tissues. The expression of HMGB1 and Ki67 was detected by immunohistochemistry. Results Database analysis showed that the expression level of FGD5-AS1 in OSCC tumor tissues was 4 times higher than that in normal tissues, and FGD5-AS1 expression was associated with poor grade in OSCC patients. Compared with normal tissues or human oral mucosal cells, the expression of FGD5-AS1 in tumor tissues and OSCC cell lines was significantly increased, and the expression of miR-129-5p was significantly decreased (P<0.05), the CAL-27 cells with the highest expression level of FGD5-AS1 were selected for transfection experiments. Compared with the Control group and the si-NC group, the apoptosis rate of the si-FGD5-AS1 group was significantly increased, and the OD value (48 h, 72 h, 96 h), scratch healing rate and the number of invaded cells were significantly reduced (P<0.05). MiR-129-5p was the target gene of FGD5-AS1. Inhibiting the expression of miR-129-5p was able to reverse the effects of interference FGD5-AS1 on the proliferation, apoptosis, migration and invasion of OSCC cells, thereby restoring the cancer-promoting effect of FGD5-AS1. After FGD5-AS1 was disrupted, HMGB1 expression was down-regulated by significantly enhancing miR-129-5p expression (P<0.05). In vivo experiments showed that FGD5-AS1 silencing significantly inhibited the growth and expression of HMGB1 and Ki67 (P<0.05), inhibition of miR-129-5p was the opposite; Inhibition of miR-129-5p reversed the inhibition of FGD5-AS1 on tumor growth and expression of HMGB1 and Ki67 (P<0.05). Conclusions FGD5-AS1 is up-regulated in OSCC cells. Interfering with FGD5-AS1 can inhibit proliferation, migration and invasion of OSCC cells and promote apoptosis by targeting miR-129-5p / HMGB1 axis.
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Behavioral assessment in the parkinson’s model of nonhuman primates

liushuyi, zhengbo wang

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Parkinson's disease is a neurodegenerative disease, can cause a series of patients with symptoms of movement and the movement, behind the pathogenesis is unclear, to explore the mechanism behind these phenotypic requires an appropriate animal model of rodents in the movement and the movement is very difficult to accurately simulate the patient symptoms, causes related to preclinical studies have limitations, in translational medicine. Non-human primate animal models can make up the gap between rodents and humans, thus the non-human primate PD model of movement and the movement symptoms, is very important to research on mechanism and therapy, this review summarizes the different behavior in quantitative way, and compared the advantages and disadvantages between different methods, for studying the PD monkey model provides a behavioral testing for help.
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Advances in the construction of animal models of severe asthma

Wei Dandan, Wang Liting, Long Jie, Chen Yanjiao, Wang Yu, Yang Yongqing, Xu Yudong

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Severe asthma (SA), which requires high doses of glucocorticoids in combination with other medications to maintain symptom control or is uncontrollable even with these treatments, is currently a challenge in the clinical management of asthma. The establishment of a stable and reproducible experimental animal model that highly mimics the pathophysiological and clinical characteristics of patients with severe asthma is a key fundamental link in deepening the study on the pathogenesis of severe asthma, identifying potential therapeutic targets and developing targeted drugs. This paper reviews the experimental studies related to the construction of animal models of severe asthma in the past 10 years, and summarizes the recent progress in the establishment and evaluation of animal models of severe asthma from three aspects: animal selection, animal model construction protocols, and model pathological phenotypes. To summarize and analyze the latest progress in the construction of SA animal models, and provide a reference for SA basic research based on animal models.
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Research progress in experimental models of pulmonary arterial hypertension

xiejincheng, Chenjianying, Dengshaodong, Xiao mengyuan

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Pulmonary hypertension is a chronic progressive disease that, if not treated promptly, can ultimately lead to right heart failure and even death In order to explore the pathogenesis of pulmonary arterial hypertension and find more effective treatment methods, it is necessary to establish a suitable experimental model. In this paper, Pubmed, CNKI and other databases were used to search relevant literature, and the preparation methods and research progress of various experimental models of pulmonary arterial hypertension in recent years were summarized. The preparation methods of the models were classified to show the pathological characteristics of the disease more directly. On this basis, the present situation and existing problems of the in vitro and in vivo model of pulmonary arterial hypertension were discussed, in order to provide reference for the pathogenesis and clinical research of pulmonary arterial hypertension.
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Research progress of experimental premenstrual dysphoria model in rodents

xujialing

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Premenstrual dysphoric disorder (PMDD) is a subtype of Premenstrual syndrome with high prevalence in women during their reproductive life. It includes physical symptoms such as breast tenderness, headache as well as serious emotional symptoms such as anxiety, depression and irritability. These symptoms are menstrual specific, they appear before menstruation and disappear within a week after it ends. PMDD threatens the health of female patients all over the world, In The Diagnostic and Statistical Manual of Mental Disorder(Fifth edition ed,DSM-5）, PMDD is identified as one of the five types of depression. At present, studies on the pathological mechanism of PMDD mainly focus on hormone and receptor expression, which is the theoretical basis of the animal model establishment, as well. Animal model that can model after clinical symptoms of human beings is a very important to connect basic research to clinical research, which is also crucial to explore the pathogenesis and develop appropriate drugs. Although many kinds of animal models of PMDD have been used in experimental studies, there are still many limitations, which resulting in a barrier to further investigation of PMDD. Therefore, this review arranged the known pathogenesis research of PMDD and discuss the existing animal models of PMDD, aims to provide reference for PMDD related mechanism research and drug development.
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Analysis of animal models of keratitis based on the characteristics of clinical conditions of traditional Chinese and Western medicine

nanshuo

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Abstract: Keratitis is a common ophthalmic disease with a high rate of blindness. This paper reviews a large number of relevant literature of animal models of keratitis, summarizes and analyzes the mechanism of existing animal models of keratitis, and evaluates the clinical anastomosis degree of traditional Chinese and Western medicine in combination with the established clinical diagnostic standards of traditional Chinese and Western medicine, analyzes its advantages and disadvantages, and puts forward some suggestions. It is found that most of the existing models are based on Western medical theories, and lack the diagnostic standards of traditional Chinese medicine. The model is mostly modeled by a single factor, which cannot well simulate the real lesion process of the disease; The diagnosis of the model lacks apparent indicators; It is recommended that animals be modeled by combining disease evidence. It is very important to prepare animal models of keratitis with high clinical compatibility and establish perfect evaluation standards, which can help us better understand the occurrence and development of keratitis in modern medical experiments, and effectively prevent and treat it.
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Study on the uptake and transport properties of euscaphic acid in Caco-2 cell model based on UPLC-TQ-MS

wangning, xieli, ding wenhuan, tian li

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ABSTRACT: Objective Caco-2 cell model was established to explore euscaphic acid uptake and transport mechanism in this study. Methods Ultra-high performance liquid chromatography-triple quadrupole-mass spectrometry(UPLC-TQ-MS) was employed to determine the content of euscaphic acid. The effects of different time and temperature on its uptake were investigated. Based on the results of the uptake studies, the effects of different concentrations, P-gp inhibitors, chelating agents and pH values on its bidirectional transport were explored. Results The uptake of euscaphic acid was (8.38 ?0.87) μg穖g-1 for 180 min on the Caco-2 cell model at 37 癈. The apparent permeability coefficient (Papp values) of euscaphic acid for low, medium and high concentrations were(61.41 ?.92)?0-4、(146.90?4.91)?0-4 and (167.18?.72)?0-4 cm穝-1 respectively, which were positively correlated with the concentrations. P-gp inhibitors and chelating agents had no effect on its Papp values. Weakly acidic environment (pH6.00) significantly increased its Papp value, and the efflux rate (ER) ranged from 0.8–1.4. Conclusion The above results indicate that euscaphic acid has good transmembrane permeability in Caco-2 cell model, and the uptake mode is mainly passive diffusion. It is not a substrate of P-gp and there is no cellular bypass transport. This research may provide an experimental basis for the in vivo intestinal absorption of medicines containing euscaphic acid.
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Mechanism of taxifolin regulating endoplasmic reticulum stress PERK-ATF4 pathway to reduce myocardial hypertrophy in hypertensive rats

yujinyu, hanjing, zhangying, yuwen

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【Abstract】 Objective To investigate the impact and molecular mechanism of taxifolin (TAX) on myocardial hypertrophy in spontaneously hypertensive rats (SHR). Methods Twenty-four SHRs were separated into SHR control group (SHR group), TAX group (20 mg/kg), and TAX PERK activator CCT020312 (CCT) group (20 mg/kg TAX 2 mg/kg CCT), 8 per group; another 8 normal blood pressure Wistar-Kyoto (WKY) rats were regarded as the normal control group (WKY group), and all were given corresponding drugs for 8 weeks of continuous intervention. During the experiment, the changes in blood pressure of the rats were observed, and after the intervention, the thickness of the diastolic ventricular septum (IVSd), the thickness of the systolic ventricular septum (IVSs), and the left ventricular ejection fraction (LVEF) were detected by echocardiography to determine the degree of myocardial hypertrophy and cardiac function, then the cardiac index and left ventricular index were calculated, hematoxylin-eosin (HE) staining, wheat germ agglutinin (WGA) staining and Masson staining were performed to evaluate the pathological changes of myocardial tissue, real-time quantitative PCR (qRT-PCR) was performed to detect the expressions of atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP), type I collagen α1 chain (COL1A1) and type III collagen α1 chain (COL3A1) mRNA in myocardial tissues, Western blot was performed to detect the expressions of protein kinase R-like endoplasmic reticulum kinase (PERK)-activator of transcription 4 (ATF4) pathway-related proteins in cardiac muscle. Results After the intervention, compared with the WKY group, the systolic blood pressure (SBP), diastolic blood pressure (DBP), IVSd, IVSs, cardiac index, left ventricular index, myocardial cell cross-sectional area, collagen volume fraction (CVF), myocardial tissue ANP, BNP, COL1A1 and COL3A1 mRNA expressions, glucose-regulated protein 78 (GRP78), ATF4, C/EBP homologous protein (CHOP) protein levels and p-PERK/PERK ratio in the SHR group increased (all P<0.05), LVEF decreased (P<0.05); compared with SHR group, the SBP, DBP, IVSd, IVSs, cardiac index, left ventricular index, myocardial cell cross-sectional area, CVF, myocardial tissue ANP, BNP, COL1A1 and COL3A1 mRNA expressions, GRP78, ATF4, CHOP protein levels and p-PERK/PERK ratio in TAX group decreased (all P<0.05), LVEF increased (P<0.05); CCT020312 partially reversed the protective effects of TAX on cardiac function and cardiac hypertrophy. Conclusion TAX can improve hypertensive myocardial hypertrophy by inhibiting endoplasmic reticulum stress (ERS), and its mechanism may be related to inhibiting PERK-ATF4 pathway.
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Study on tissue distribution difference of ligustrazine-Salvia miltiorrhiza before and after compatibility in acute myocardial ischemia model rats

lirong, goujian, liuting, gongzipeng, luyuan, liuchunhua, hunagyong, sunjia

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Objective To investigate the difference in tissue distribution of ligustrazine hydrochloride and Salvia miltiorrhiza (Danshen) in Acute myocardial ischemia (AMI) rats. Methods AMI model was induced by subcutaneous injection of isoproterenol hydrochloride. UPLC-MS/MS method was used to determine the content differences of ligustrazine and danshensu in heart, liver, spleen, lung, kidney and brain tissues after single intravenous injection of Danshen injection (DGI), Ligustrazine injection (CGI) and Shenxiong glucose injection (SGI) at different time points. Results After intravenous injection, ligustrazine and danshensu were widely distributed in tissues of AMI rats and reached their peak rapidly. Before and after compatibility, the content of ligustrazine was the highest in brain tissue and the lowest in liver tissue. The content of danshensu in kidney tissue was the highest, and in brain tissue was the lowest, indicating that ligustrazine could penetrate the blood-brain barrier more easily than danshensu, and the main accumulation tissues were different. The AUC of ligustrazine and danshensu in the heart of the target organ was significantly increased (P < 0.001). Conclusion It is speculated that the combination of ligustrazine and salvia miltiorrhiza may enhance the therapeutic effect by increasing the distribution of main pharmacodynamic components in the heart, so that SGI can play a better role.
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The role of PI3K/Akt/mTOR signaling pathway in the pathogenesis of TRALI rats

liushuangchun, Zhang Xijiang, Chen Zaihuan, Wang Luqian, Lin Hairong

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Objective: To study the effect of PI3K/Akt/mTOR signaling pathway on the pathogenesis of TRALI. Methods: Animal model was established by the method of trauma-blood loss-massive transfusion, and the pulmonary histopathological changes were detected by HE staining to determine whether the rats had pulmonary edema. The protein and mRNA expression levels of TNF-α, IL-6 and IL-1β in peripheral blood or lung tissues in TRALI rat models were detected by ELISA and qRT-PCR. The expression levels of PI3K/Akt/mTOR signaling pathway related proteins and apoptosis-related proteins Bax, Bcl-2 and Caspase3 were detected by western blotting. Results: Alveolar tissue structure was seriously damaged, the alveolar wall was thickened, there was pink edema fluid in the alveolar cavity, inflammatory cells infiltrated, edema was obvious in TRALI model rat. The expression levels of inflammatory cytokines TNF-α, IL-6 and IL-1β were significantly increased in peripheral blood and lung tissues (P<0.05); PI3K/Akt/mTOR signaling pathway was activated, the expression of p-mTOR/mTOR was significantly increased, and the expression of apoptotic protein Bax and Caspase 3 was inhibited, and the expression of anti-apoptotic protein Bcl-2 was increased (P<0.05). Conclusion: As a potential drug target, mTOR is an important means for clinical prevention and control of the occurrence and development of TRALI by defining the exact time target of its protective and damaging effects and selecting the optimal time of medication due to its complicated mechanism.
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Alterations of Gut Microbiota - Short Chain Fatty Acid Axis in IBS-D Rats and the Effect of Sodium Butyrate

zhan kai, Wu haomeng, zheng huan, qin shumin, Huang shaogang, yang yuanming

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Objective To explore the alterations of gut microbiota - short chain fatty acid metabolic axis in IBS-D rat model, and to explore the effect of sodium butyrate on this axis. Methods Seventeen Wistar rats were randomly divided into three groups. The IBS-D rat model was induced by 4% acetic acid enema combined with restraint stress. During the modeling period, sodium butyrate was injected intraperitoneally. The fecal flora of rats was detected by 16sRNA technology, and the fecal short chain fatty acid content of rats was detected by liquid chromatography mass spectrometry (LC-MS). Results Compared with the normal group, the weight of the model group was decreased, AWR score and fecal water content have a significant increase, the relative abundance of intestinal probiotics was decreased，while that of g-Blautia was elevated, the fecal acetic acid content was increased significantly, and the contents of butyric acid and valeric acid was decreased significantly in the model group. After drug intervention, compared with the model group, the weight of rats in the sodium butyrate group was increased, the AWR score and fecal water content was decreased significantly, the relative abundance of g-Blautia was decreased significantly, and the fecal butyric acid and valeric acid content was obviously increased. Conclusions Sodium butyrate can alleviate diarrhea and colon visceral hypersensitivity in IBS-D rats by improving the imbalance of gut microbiota - short chain fatty acid metabolic axis.
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Advances in Ferroptosis-Based Therapy for Aging and Aging-Related Diseases

Zhou yongchang, Tao Siman, Chen Shengqiang, Pu Xiuying

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Ferroptosis is a novel form of programmed cellular necrosis proposed in recent years, which is found in various diseases and seriously impacts on human health. Numerous studies have shown that inhibition or promotion of ferroptosis can improve many aging and aging-related diseases, and Traditional Chinese medicine plays an important role in this regard. This paper reviews the effects and mechanisms of Ferroptosis on aging and aging-related diseases, and compares the research progress of TCM in the treatment of ferroptosis-mediated aging and aging-related diseases in recent years, aiming to provide more options for the treatment and prevention of aging and aging-related diseases.
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Research progress in the pathogenesis of inflammatory bowel disease

Houxiaoting, Menghuan, Xuejiachen, Zhanghuamin, Wangkesi, Wangxude

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Inflammatory bowel disease (IBD) is a global idiopathic disease, involving the ileum, rectum and colon. IBD begins to appear early in clinical symptoms, including abdominal discomfort, diarrhea, hematochezia, fever, fatigue and weight loss. The diagnosis of IBD is based on the comprehensive evaluation of relevant clinical manifestations, endoscopic examination results and histopathological characteristics of pathological tissue specimens. Biological agents, oral corticosteroids, salicylic acid and surgery are the main conventional treatments for IBD. In recent years, considerable progress has been made in elucidating the pathogenesis of IBD. In clinical practice, it is considered that the complex interaction between genetic susceptibility, environmental factors and intestinal mucosal barrier leads to abnormal oxidative stress, autophagy and mucosal immune response. This paper briefly summarizes and expounds the research progress of genetic and environmental factors, intestinal mucosal barrier function, oxidative stress, autophagy dysfunction and adaptive immune response, so as to provide basis for further research and development of treatment methods and improvement of clinical treatment effect.
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Effect of Bushen Jianpi Kaixin formula on autophagy and apoptosis in AD rats

li ying, Wang Ying, Kong Mingwang

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Objective To investigate the effects of Bushen Jianpi Kaixin Formula (BSJPKXF) on the learning and memory ability of Alzheimer s disease (AD) model rats and the related autophagy and apoptosis in cortex of AD model rats, and exploring the underlying mechanism of BSJPKXS. Method The 60 eligible rats were randomly divided into six groups (n = 10): control group, AD group, Bushen group (BS, 3.6g/kg·d), Jianpi group (JP, 4.05g/kg·d), Kaixin group (KX, 2.34g/kg·d) and Bushen Jianpi Kaixin group (BSJPKX, 9.99g/kg·d). AD mouse model was established by intraperitoneal injection of D-gal. The rats in BS group, JP group, KX group and BSJPKX group were gavaged with corresponding drugs once a day. The rats in control group and AD group were treated with equal amount of normal saline one time per day. After four weeks, the learning and memory ability was tested by Morris water maze. The open-field test was used for detecting the cognitive function in rats. The expression of LC3-I, LC3-II and Beclin in cerebral cortical tissues were detected by western bolt. The expression of Bax and Bcl-2 in cerebral cortical tissues were detected by immunohistochemistry. The related mRNA level of Beclin 1, P62, Bax and Bcl-2 in cerebral cortical tissues were detected by RT-PCR. Result Compared with the control group, D-gal significantly decreased the spatial learning and memory ability of rats in the AD group (P < 0.01), decreased the expression of Beclin, LC3-I/LC3-II, Bcl-2 and Bcl-2/Bax, increased the mRNA level of P62 and the expression of Bax (P < 0.01). After treatment, related to the AD model group, Bushen Jianpi Kaixin formula improved the spatial learning memory ability of rats in the BSJPKX group (P < 0.01), increased the expression of Beclin, LC3-I/LC3-II, Bcl-2 and Bcl-2/Bax, decreased the mRNA level of P62 and the expression of Bax (P < 0.01). Conclusion Bushen Jianpi Kaixin formula can improve cognitive impairment in AD rats. The mechanism is presumedly related to the reduction of neural autophagy and apoptosis.
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The evaluation of experimental animal studies on acupuncture for hypertension based on the SYRCLE’s tool and the ARRIVE guidelines

Tang wenjing, ZHANG Yue, LI Yuxi, ZHONG Dongling, JIN Rongjiang, ZHANG Lili, LI Juan

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Objective To evaluate the risk of bias and reporting quality of animal experimental studies on acupuncture for hypertension, and analyze the deficiencies in experimental design, implementation and reporting, so as to decrease the risk of bias of researches and improve the reporting quality of animal studies. Methods Databases including China national knowledge infrastructure（CNKI）, Wanfang database（WANFANG）, Chinese science and technology periodical database（VIP）, Chinese biomedical literature database（CBM）, Web of Science, PubMed, Embase, and The Cochrane Library were searched from inception to October 8, 2022. Two researchers independently screened experimental studies related to acupuncture interventions in hypertensive animals according to eligibility criteria. The SYRCLE’s tool and the ARRIVE guidelines 2.0 were used to evaluate the risk of bias and reporting quality of the included literature. Excel 2019 was used to extract data and descriptive analysis was conducted according to the results. Results A total of 79 animal experiments on acupuncture for hypertension were included, among which 16 and 21 were published in Chinese core journals and science citation index（SCI）journals respectively. The result of SYRCLE’s tool showed that 5 of the 10 items were evaluated as well, while the rest were unclear risk or high risk of bias. Of the 79 included articles, the risk of bias of 19 articles were low, while the remaining studies had some risk of bias. The results of the ARRIVE guidelines 2.0 indicated that 19 of the 38 sub-items were well reported, while the rest were poorly reported.The reporting quality of 51 articles were good and the remaining studies were inadequately reported. Conclusions At present, the risk of bias of acupuncture intervention in hypertensive animal experiments is high and the reporting quality is generally low. The inadequate description of some important entries had impact on the reproducibility of the experiments and the translation of the results.The SYRCLE’s tool and ARRIVE guidelines 2.0 are recommended to be used as reference during experimental design and reporting, thus improving the standardization and reporting quality of acupuncture for hypertensive animals.
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Autophagy: the key mechanism of exercise in improving neurodegenerative diseases

Chen Xianghe, Qiu Xiao, Liu Chi, Shen Ziming, Zhou Xiangxiang

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Autophagy regulation of neurological diseases is the focus of current research in the field of neuroscience. Autophagy disorder leads to protein expression, deposition and dysfunction such as Aβ、Tau、α-syn and causes neurodegenerative diseases such as AD, PD and HD. Exercise is an important means to improve neurodegenerative diseases, which is closely related to the up-regulated expression of LC3, Beclin-1, Lamp1 and other autophagic factors after the activation of AdipoR1/AMPK/TFEB, AMPK/mTOR and other pathways. Higher autophagy level can remove the deposition of Aβ、Tau、α-syn and other proteins in the brain and can improve the neurodegeneration, synaptic structure and function disorder caused by neurodegenerative diseases. This study reviewed and analyzed the mechanism of autophagy in the improvement of neurodegenerative diseases by exercise, which will provide a solid theoretical basis and new research ideas for the improvement of neurodegenerative diseases by exercise.
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guojia

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Editor Sun

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Research advances of trophoblast cells in threatened abortion complicated with intrauterine hemorrhage

HuoYan, Zhu Jun nan, Fu Ya qi, Chen Ping, Xu Guang li

Abstract: (741) HTML (0) PDF (0.00 ByteKB) (0)

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Threatened abortion complicated with intrauterine hemorrhage is a common disease during pregnancy.Its pathogenesis is related to the imbalance of maternal-fetal interface microenvironment and the obstruction of uterine spiral artery remodeling. Trophoblast cells are the outermost layer of the maternal-fetal interface microenvironment .Its proliferation, migration and invasion are closely related to normal pregnancy.It plays an irreplaceable role in immune tolerance and regulation, uterine spiral artery remodeling, and maintenance of maternal-fetal interface microenvironment.In recent years, trophoblast cells have become the main line of research in autoimmune diseases and other fields.Studies have found that it plays an important role in the diagnosis and treatment of threatened abortion complicated with intrauterine hemorrhage.This article reviews the research progress of trophoblast in the treatment of threatened abortion complicated with intrauterine hemorrhage.
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SUNYE

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yiyi

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The mechanism of chemotherapy-induced thrombocytopenia in hematological malignant tumors

liliang, kong chun fang, jin cheng hao

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Chemotherapy is the main cornerstone of hematological tumor therapy. However, foot therapy and high-dose chemotherapy drugs often cause bone marrow hematopoiesis inhibition, among which thrombocytopenia is more common, which can increase the risk of bleeding, delay follow-up treatment, increase treatment costs, and even endanger life. In recent years, more and more studies have found that anti-tumor drugs can mediate thrombocytopenia through cell aging, apoptosis, autophagy and ferroptosis. Therefore, this article reviews the mechanism of chemotherapy-induced thrombocytopenia in hematological malignant tumors in recent years.
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Volume 36,2026 Issue 2

Volume 36,2026 Issue 2

Volume 36,2026 Issue 2

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