Abstract: 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 how Gli2 regulation affects the migration and invasion of oral cancer cells. Methods Small interfering ( si)RNA 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 assays were used to explore the mechanism of how Gli2 regulation effects the malignant proliferation and metastasis of Tca8113 cells. Results The mRNA and protein expression of Gli2 in oral cancer cells ( Tca8113) increased. Interference of Gli2 expression inhibited the proliferation, growth, migration, and invasion of Tca8113 cells. Further experiments showed that interfering with Gli2 expression inhibited the mRNA and protein expression of key factors in the Hedgehog ( Hh) pathway. In addition,interference of Gli2 expression significantly affected the mRNA and protein expression of key factors in epithelial mesenchymal transformation ( EMT) pathways. Conclusions Gli2 is abnormally activated during oral cancer, and interference of 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 the Hh and EMT pathways. This study has provided a new way to elucidate the pathogenesis of oral cancer and new perspectives on the clinical treatment of oral cancer.

Abstract: Objective To study the potential harmful effects of brake-pad sourced particles. Methods Grind the brake pad particles or antimony sulfide particles. Mice were exposed brake pad or antimony sulfide particles by tracheal perfusion for 1 month. We observed pathological changes to the lungs, heart, and liver, and analyzed changes in peripheral blood macrophages and regulatory T cells (Tregs) via flow cytometry. Results After exposure, the deposition of foreign substances in the alveolar wall of mice was seen, with the obvious infiltration of inflammatory cells around blood vessels,which worsened with increasing particle concentration. 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, in the antimony sulfide group and low-dose brake pad particle group. Conclusions Exposure to brake pad particles and their component antimony sulfide has varying degrees of toxic effects on the lung,heart, and liver of mice and has an impact on the immune system, indicating the potential health hazards of brake-padderived air pollution.

Abstract: Objective By employing surgically induced varicocele (VC) in SD rats and an apomorphine (APO) test, we screened rats with erectile dysfunction ( ED) after VC and explored method to establish VC and ED models. Methods Sixty rats were randomly divided into Control, Sham, and Model groups with 20 rats in each group. Using the Turner method , we partially ligated the left renal vein to induce left VC three times. APO tests were conducted to screen rats with ED after inducing VC. The numbers of erections, genital grooming, and yawning were observed and recorded.The diameter of bilateral spermatic veins were measured. Both testises and kidneys were weighed. HE staining was used to observe pathological changes of penis and left testis. The success rate of modeling was calculated in the Model group. Results A VC and ED model was successfully established in 15 out of 20 rats in the Model group with a success rate of 75%. After modeling, the diameter of the left spermatic vein in the model group was increased significantly(P<0. 01) and was significantly larger than that before modeling(P<0. 01). The diameter of the right spermatic vein in the Model group was increased(P<0. 05) and higher(P<0. 05) than that before modeling. The weight of the left testis in the Model group was significantly decreased(P<0. 01) compared with that of the right testis. No significant difference in the bilateral kidney weights were observed between or within groups(P<0. 05). In the Model group, the numbers of erections, yawning, and genital grooming decreased significantly(P<0. 01) with the time of modeling. Pathological changes of the left testis and penis were significant in the Model group. Conclusions The Turner method increases the diameter of the spermatic vein in rats, causing testis injury and weight loss, and APO tests can be used to screen rats with ED after VC induction. The combination of the two method is suitable to establish an animal model of VC with an ED status similar to humans.

Abstract: Objective To explore the effect of decoction of Euphorbia fischeriana Steud. and jujuba (DEFSJ) against estrogen receptor (ER) negative (-) and ER positive (+) breast cancer via the PI3k / Akt pathway, and to provide a reference for the targeted treatment of breast cancer. Methods DEFSJ extract was prepared and analyzed using UHPLCTriple Quad. DEFSJ containing serum (CS) was prepared via a serum pharmacology method . Different concentrations of DEFSJ-CS were applied to (ER-) MDA-MB-453 and (ER+) MCF-7 breast cancer cells in vitro for 48 h. The distribution of cells in different stages of the cellular cycle was evaluated using a Flow cytometer. DNA ladder assay was used to assess the degree of apoptosis, and the expression of PI3k / Akt pathway-related proteins was evaluated by Western blot assay. The expression of FoxO3a, FoxO1a, and Bim mRNA was detected by Real-time quantitative PCR. Nuclear transposition of FoxO3a protein was analysed using a confocal laser microscopy. Results Five batches of DEFSJ extract were analyzed using UPLC, and the result showed that the preparation technology was feasible and the quality was controllable, ensuring the accuracy of the pharmacological experiment result. DEFSJ-CS blocked cells in the G2 / M phase (P<0. 05, P<0. 01).Cells treated with DEFSJ-CS displayed the typical apoptotic ladder in the DNA ladder experiment. Compared with the negative control cells, the DEFSJ-CS group cells had decreased protein expression of p-PI3k, p-Akt, p-FoxO3a, and pFoxO1a (P<0. 05, P<0. 01); increased protein expression of Bim (P<0. 05); decreased mRNA expression of FoxO3a and FoxO1a ( P<0. 05,P<0. 01); increased mRNA expression of Bim ( P<0. 05,P<0. 01); and enhanced nuclear translocation of FoxO3a protein. The data showed that DEFSJ-CS had a stronger effect on (ER-) MDA-MB-453 cells than (ER+) MCF-7 cells. Conclusions The regulatory effect of DEFSJ extract on anti-breast cancer involves the PI3k / Akt pathway, and the effect varies with phenotypic differences.

Abstract: Objective To study the core behavioral symptoms, biological indicators, and pathological changes of a mouse model of breast cancer complicated with depression induced using 4T1 breast cancer cell inoculation combined with chronic restraint stress (CRS). Methods BABL/ c mice were randomly divided into Control, Stress, Tumor, and stress combined with tumor (S+T) groups. Mice in the tumor and S+T groups were inoculated under the front legs with breast cancer 4T1 cells. After tumor formation, mice in the stress and S+T groups were subjected to CRS for 21 days. The body weight and food intake of each group were monitored during modeling. After the experiment, the occurrence of depressionlike 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 weights and volumes of the tumors were measured.Concentrations of serum tumor markers, including carbohydrate antigen (CA199), carcinoembryonic antigen (CEA), and vascular endothelial growth factor ( VEGF), and related neurotransmitters, including 5-hydroxytryptamine ( 5-HT),norepinephrine ( NE), and corticosterone ( CORT), were determined using ELISA. HE staining was used to observe histopathological changes to the hippocampus and tumor. Results In S+T group mice, body weight and food intake were significantly decreased, tumor weight and volume were significantly increased, serum tumor marker ( CA199, CEA,VEGF) levels were significantly increased, enthusiasm and desire to explore a new environment were reduced, stress and despair behaviors were significantly increased, and levels of the serum neurotransmitters 5-HT and NE and levels of CORT were significantly increased. In addition, the cell arrangement in the tumor tissue was loose, the amount of intercellular substance decreased, the pathological nuclear classification phase was increased, the arrangement and morphology of neurons in the CA3 region of the hippocampus were disordered, and there were obvious nuclear vacuolation-like changes. Conclusions A mouse model of breast cancer complicated with depression induced by 4T1 breast cancer cell inoculation combined with CRS showed the typical dual symptoms and biological indicators of breast cancer and depression and can be used as a good reference model for experimental studies of breast cancer complicated with depression.

Abstract: Objective A stable model of acute obstructive suppurative cholangitis was established in rats to detect pathophysiological indexes and provide a 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 via the injection of toxoid into the lower bile duct, followed by ligation of the common bile duct. 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. There were no deaths and no abnormalities of liver function in the sham-operation group. Three rats died in the model group, and the mortality rate of the model group was 12%. The main indexes of liver function and liver pathology showed obvious cholestasis and injurious changes to hepatic function in the model. Conclusions In this study, an acute obstructive suppurative cholangitis model rat was successfully established. The model has the advantages of ease of operation, minimal injury, low mortality, and a highly successful modeling rate, and it can provide a standardized experimental animal model for studying the mechanisms of and developing drugs for these common diseases.

Abstract: Objective This study aimed to investigate the therapeutic efficacy of Sanjie Quban recipe in a keloid nude mice model and its impact on transforming growth factor-β1 ( TGF-β1). Methods Keloid tissue after surgical resection was subcutaneously transplanted into the backs of healthy SPF BALB/ C female nude mice, aged 6~ 8 weeks, and a keloid nude mice model was thus established. The mice were randomly divided into three groups, the Sanjie Quban recipe group,the Asiaticoside tablet group and the control gnup, with five in each group. They were respectively treated with Sanjie Quban recipe, Asiaticoside tablets, or sterile pure water. After 28 days of continuous gavage, the keloid tissue was exfoliated and weighed, and HE staining, Masson staining, and immunohistochemical staining for TGF-β1 were conducted.Differences in keloid weight between the three groups before and after treatment were compared, as were the differences in collagen fiber, fibroblast numbers, and TGF-β1 expression between the three groups after treatment. Results The difference in keloid weight before and after treatment in the Asiaticoside tablet group was greater than that of the control group, and the weight difference before and after treatment keloid treatment was the largest in the Sanjie Quban recipe group (P<0. 01). Compared with the control group, collagen fibers in the Sanjie Quban recipe group were looser and less numerous, and fibroblasts were decreased in number. The expression of TGF-β1 in the Sanjie Quban recipe group was decreased compared with that of the control group (P<0. 01). Conclusions Sanjie Quban recipe has certain therapeutic effects on keloids. The mechanism may involve reducing the expression of TGF-β1 in keloid tissue and thereby reducing the proliferation of fibroblasts and the synthesis of extracellular matrix. This study provides experimental and theoretical bases for the clinical treatment of keloids with Chinese medicine.

Abstract: Objective To explore the action of Bufei Jianpi formula (BJF) on mitochondrial damage to skeletal muscle in chronic obstructive pulmonary disease ( COPD) rats via its regulation of the IRS-1/ PI3K signaling axis. Methods 60 SPF SD rats were randomly divided into Control group, Model group ( COPD stable stage group ),aminophylline (Am) group, BJF group, pioglitazone (PIO) group and BJF+PIO group, with 10 rats per group. A stable COPD rat model was established via forced smoking and Klebsiella pneumoniae nasal drip method. Samples were taken from the 9 the week to the end of the 20 the week, and the weight of the rats was measured every week. Routine sectioning and HE staining were performed on lung and skeletal muscle tissue, and corresponding pathological changes were observed under a light microscope. The lung function of the rats was observed by whole-body plethysmography in weeks 0, 8, and 20,including tidal VT, PEF, and 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 Western blot. Results The Model group, but not the Control group, showed a large number of inflammatory cells infiltrating the alveolar interstitium and bronchus, indicative of lung disease; some alveolar walls had broken and fused to form air cavities, and fiber networks were destroyed. After drug treatment, the rats showed improved alveolar wall and fiber network integrity and reduced inflammatory cell infiltration in the bronchus, especially those in the BJF and Am groups. In the drug treatment groups, the skeletal muscle pathology of each group showed improved spatial arrangement, the atrophy and fracturing of muscle fibers were ameliorated to different degrees, and cytoplasmic staining of muscle cells was uneven, and the BJF group showed the most significant effects. Compared with the Control group, the Model group’s PEF, VT, and EF50 significantly decreased from week 8 (P<0. 01), while the BJF, BJF+PIO and Am groups had significantly increased PEF and EF50 (P<0. 01). Compared with Control group, the Model group’ s mRNA and protein expression levels of IRS-1, PGC-1α, and PI3K were significantly decreased (P<0. 05, P<0. 01) , the level of leptin was significantly increased (P<0. 01). Compared with the Model group, the mRNA and protein expressions of IRS1, PGC-1α and PI3K in the BJF group were significantly increased (P<0. 05, P<0. 01), and the mRNA expression of IRS-1 in the PIO group was significantly increased (P<0. 01). The BJF+PIO group’s mRNA levels of PGC-1α (P<0. 01) and mRNA and protein levels of IRS-1 and PI3K were significantly increased (P<0. 05, P<0. 01). The mRNA and protein expression levels of PI3K in the Am group were significantly increased (P<0. 01). The expression levels of leptin mRNA were significantly decreased in the four treatment groups (P<0. 01), and the expression of leptin protein was significantly decreased in all treatment groups except the Am group (P<0. 01). Compared with the Control group, the Model group’ s quadriceps femoris tissue showed a significant decrease in TFAM and p-AKT expression. TFAM and p-AKT expression in all the treatment groups showed an increasing trend, but the difference was not statistically significant ( P> 0. 05). Conclusions By regulating the IRS-1/ PI3K signaling axis, Bufei Jiempi reduces mitochondrial damage to skeletal muscle, increases the expression of PGC-1α and mitochondrial transcription factor TFAM, enhances mitochondrial biosynthesis, and reduces pathological damage to lung and skeletal muscle tissue.

Abstract: Objective To investigate whether a stable and reliable hyperuricemia model can be established in mice with an ICR background via a triple-modeling method ( combined potassium oxazine, hypoxanthine, and 30% yeast paste), and to evaluate the effect of the positive drug febuxostat on the model. Methods A hyperuricemia model of ICR mice was established using a single drug or double- or triple-drug combinations. Serum uric acid and creatinine concentrations, xanthine oxidase (XOD) and urate oxidase (UOX) activity, and uric acid transporter (URAT)1, glucose transporter (Glut)9, anion transporter (OAT)1, and ATP-binding box subfamily G member (ABCG)2 mRNA levels were detected to evaluate whether the hyperuricemia model was formed successfully. Results The serum uric acid levels of ICR mice were not significantly changed by potassium oxazine alone, as they showed an increase but were not significantly different to those of the 30% yeast paste diet or hypoxanthine combined groups. Serum uric acid levels in the triple administration group were significantly increased at 7 days (P<0. 01), while XOD enzyme activity had increased(P<0.01) and UOX enzyme activity decreased (P<0. 001) at the same timepoint. There were increased expression levels of URAT1 and Glut9 (P<0. 05, P< 0. 001), and decreased expression levels of OAT1 and ABCG2 (P<0. 001). During dynamic monitoring, the blood uric acid levels of triple administration-induced ICR mice peaked at 7 days. In addition,triple administration-induced hyperuricemia in ICR mice was sensitive to the positive drug febuxostat, which caused a significant decrease in blood uric acid levels ( P< 0. 001). Conclusions A hyperuricemia model in ICR mice can be stably induced by triple administration for 7 days.

Abstract: Objective To explore the mechanisms 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 A middle cerebral artery occlusion / reperfusion ( MCAO/ R) model in rats was established via wire embolization method .PeriCam PSI laser speckle flow imaging was applied to detect whether the model was successfully established. Neurological deficits in the rats were evaluated by Zea Longa score, and histopathological changes in the rat brain were observed by HE staining. The degree of brain edema was detected by the dry and wet weight method. BBB permeability was detected by Evans blue staining, and ultrastructural changes to the BBB were observed by transmission electron microscopy. The levels of ROS, MDA and SOD activities, which are related to oxidative stress, were detected using kits. The expression levels of matrix metalloproteinase-9 (MMP-9) were detected by immunohistochemical staining and Western blot. The expression levels of Occludin, ZO-1, and Claudin-5 tight junction proteins were determined via immunofluorescence and Western blot. Results BYHWD reduced neurological deficit scores, alleviated brain histopathological damage, alleviated BBB structural disruption, prolonged the appearance of dense regions in the tight junction structure, attenuated edema of the brain on the ischemic side, and reduced BBB permeability in MCAO/ R rats. BYHWD decreased the levels of ROS and MDA,increased the activity of SOD, decreased the expression levels of MMP-9, and increased the 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 mechanisms may be related to its antioxidant activity and inhibition of MMP-9 activation.

Abstract: Objective By investigating the effects of miR-379-5p on the proliferation, invasion and metastasis of mouse breast cancer 4T1 cells, we aimed to provide new therapeutic targets for the 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 fluorescence quantitative PCR. While 5-ethynyl-2’ doxyuridine (EdU) cell proliferation and Transwell assays were employed to detect changes in the proliferation and invasion ability of 4T1 cells in each group.The migration ability of 4T1 cells after overexpression and knockdown of miR-379-5p was examined by scratch healing assay. A transplanted tumor model of breast cancer was established in BABL/ c mice, and the effects of overexpressing miR-379-5p on tumor growth and the number and size of lung metastases were observed. Results EdU result showed that knocking down miR-379-5p enhanced the proliferation ability of the cells compared with the control group cells, and miR379-5p overexpression reduced the capacity of breast cancer cells to proliferate (P<0. 05). Transwell and wound healing assays showed that miR-379-5p knockdown enhanced, while miR-379-5p overexpression significantly inhibited, the invasion and migratory ability of breast cancer cells (P<0. 01). An in vivo tumorigenesis experiment with BABL/ c mice showed that miR-379-5p overexpression significantly slowed the tumor growth rate (P<0. 05) and inhibited lung metastasis (P < 0. 01). Conclusions MiR-379-5p plays a role in tumor gene suppression in breast cancer and inhibits the proliferation, invasion, and migration of mouse breast cancer 4T1 cells.

Abstract: Objective A comparison of two method of establishing pressure ulcer rat models to determine which is the most suitable for experimental use. Methods 18 male SD rats were randomly divided into control ( n= 6), model A (n= 6) and model B (n= 6) groups. In the control group, iodophor treatment was given after hair removal at the simulated modeling site. In model group A, longitudinal compression was performed by simple deep-tissue foreign body implantation.In model group B, transverse compression was performed via the magnet compression method. The times required to complete the process and for each stage of pressure ulcer model establishment in each group were recorded. The general condition of the rats was observed, and the modeling rate, mortality rate, and infection rate were compared. Results By naked eye, we observed that the model A and model B groups gradually developed redness and swelling, ulceration,bleeding, exudation, and necrosis. Comparison of the whole time to produce pressure uler between model A and model B groups:the difference between the two groups was statitically significant (P<0. 05). Comparison of the time to produce pressure injury between Model A and Model B: The difference between the two groups at stage I was not statistically significant (P>< 0. 05); the difference between the two groups at stage II was statistically significant ( P< 0 05); the difference between the two groups at stage III was statistically significant (P<0 05); the difference between the two groups at stage IV was statistically significant P< 0 05). The mental and sports scores of the rats in the control group were significantly different from those in the model A and model B groups (P<0. 05). The general state of rats in the model group A was significantly different from that in the model B group, and coat color was dimer and activity decreased in the model group A. The modelling rate of rats in both model A and model B groups was 100%. The mortality and infection rates of the model group A were higher than those of the model group B, which were 33. 34% and 16. 70%, respectively. Conclusions Successful preparation of a four-stage model of pressure ulers in both modalities. The two method have both commonalities and distinct characteristics. The magnet compression method required less time, the rats were generally in good condition, and the mortality and infection rates were low; thus it is suitable for short-term intervention research. The simple deep-tissue foreign body implantation method took longer, required rats to have a certain level of tolerance, had high infection and mortality rates, and is more suitable for use for long-term observations of pressure ulcers.

Abstract: Objective Emergency technology research projects have two key aspects, “ emergency ” and“research”, but it is not always clear how to effectively achieve the desired result. Organizations that undertake emergency technology research projects need to develop reasonable project management mechanisms to ensure their successful implementation. In this study, we investigated the current problems faced by those managing emergency technology research projects in the medical field. We researched and analyzed possible measures to improve the efficiency and quality of scientific research management. Methods This study leveraged the author’s practical experience to investigate the current status of scientific research management in relevant units. Questionnaire surveys were conducted to ascertain the management aspects that most concern scientific managers and researchers. The problems raised by the survey were categorized and discussed. Results Through the research, we found that ( 1) at present, there are few management standards for emergency technology research projects; ( 2) the issue of greatest concern for scientific researchers is administrative approval and project funding; (3) the issue of greatest concern 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. Conclusions Emergency technology research projects have unique characteristics distinct from those of conventional technology projects. Management optimization can be carried out in terms of project approval, funding use, resource allocation, and safety. This study has provided innovative solutions to improve the management of emergency technology research projects and a useful reference of the experiences of various scientific research units in managing such projects.

Abstract:Autophagy is the main degradation and recycling pathway for abnormal aggregates and damaged organelles in cells, and it maintains the normal metabolic balance and material renewal in cells. Autophagy has neuroprotective effects and can affect the functional state of the nervous system by regulating 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 mechanisms of autophagy in nervous system diseases is of great significance for their prevention and treatment. This paper mainly reviews the current progress of autophagy research and the above diseases of the nervous system, providing a reference for further research into these diseases.

Abstract:The psychoactive properties of cannabinoids are well known, and there are controversies over whether cannabinoids can be used for therapeutic purposes worldwide. Δ⁹-tetrahydrocannabinol ( THC) is the main psychoactive substance in cannabis. The neurological mechanisms of THC were only recently discovered, and its neurological mechanism of action is still not fully understood. The blood-brain barrier (BBB) is a very important structure protecting the brain and is the first line of defense preventing foreign substances from 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 its effect and mechanism of action on the BBB, and provide a theoretical basis for studies elucidating the neural mechanism of THC.

Abstract:Transent receptor potential(TRP) channels are non-selective cation channels. In recent years, a large number of studies have found that TRP channels participate in a variety of cardiovascular diseases. How mitochondrial function is regulated by TRP channels and the relationship to cardiovascular diseases have become research hotspots. Up to now, related studies have mainly focused on TRPV, TRPM, and TRPC channels. This review focuses on the roles of the above TRP channels in the regulation of mitochondrial function and their relationships to cardiovascular diseases.

Abstract:Glutamate is a major excitatory neurotransmitter in the central nervous system and a potential neurotoxin. During the development of depression, the glutamate concentration increases in the hippocampus. When glutamate accumulates, it causes serious damage to neurons and brain tissue, aggravating the depressive state. Therefore,glutamate accumulation may be a major mechanism of depression development. Astrocytes, glutamate transporters, and glutamate receptors play important regulatory roles in the glutamate concentration. This article reviews the mechanism-ofaction of traditional Chinese medicine on depression by regulating astrocytes, glutamate transporters, and glutamate receptors, and provides new ideas to explore treatment of depression by traditional Chinese medicine.

Abstract:Apoptosis inhibitor of macrophage (AIM) belongs to group B of the scavenger receptor cysteine richsuper family. AIM is a soluble protein secreted by macrophages. The expression of this protein is controlled by the liver X receptor. AIM, which is secreted by macrophages, plays important and broad roles in the immune responses of the body. It not only inhibits the apoptosis of macrophages but also participates in the regulation of macrophage polarization. In addition, studies have revealed that AIM is involved in various physiological and pathological processes, such as inflammation, obesity, atherosclerosis, and cancer. It has been used as a biological marker for the diagnosis of diseases such as tuberculosis and liver cirrhosis. Moreover, it can promote the 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 review the multiple functional characteristics of AIM and its effects on inflammation, lipid metabolism, and related diseases to provide a theoretical basis for relevant medical research.

Abstract:Premature ovarian insufficiency (POI), also known as “ ovarian insufficiency”, has an incidence of 1% ~ 5%. The incidence has been on the rise in recent years, seriously affecting women’s physical and mental health and quality of life. At present, the cause and mechanisms of POI are still unclear, and the method and applications of model construction are also confusing. Most models have some shortcomings in pertinence and stability. The limitations greatly limit research into the clinical diagnosis and treatment of POI. This paper summarizes and discusses the etiology and pathogenesis of POI and the construction of POI animal models to provide a comprehensive reference for those studying POI.

Abstract:Post-stroke cognitive impairment ( PSCI) is a common complication after stroke, which significantly affects quality of life. However, the pathogenesis has not been fully explained. Increasing evidence has shown that the mechanism of programmed cell death (PCD) is related to PSCI, including apoptosis, necroptosis, pyroptosis, PANoptosis, parthanatos, and ferroptosis. Therefore, it is crucial to clearly understand the various mechanisms of PCD and their relationship with PSCI, and to elucidate the role of PCD in PSCI pathogenesis. The article reviews six PCD pathways related to PSCI, summarizes their mechanisms of action in PSCI, and elucidates the possible crosstalk among pathways to provide a basis for clinical targeting of regulatory factors in the PCD pathway for PSCI treatment.

Abstract:Post-stroke cognitive impairment ( PSCI) is a common complication after stroke, which significantly affects quality of life. However, the pathogenesis has not been fully explained. Increasing evidence has shown that the mechanism of programmed cell death (PCD) is related to PSCI, including apoptosis, necroptosis, pyroptosis, PANoptosis, parthanatos, and ferroptosis. Therefore, it is crucial to clearly understand the various mechanisms of PCD and their relationship with PSCI, and to elucidate the role of PCD in PSCI pathogenesis. The article reviews six PCD pathways related to PSCI, summarizes their mechanisms of action in PSCI, and elucidates the possible crosstalk among pathways to provide a basis for clinical targeting of regulatory factors in the PCD pathway for PSCI treatment.