Abstract:To compare the characteristics of the chronic constriction injury model in SD rats inducedby Minor and classic CCI, and to provide a reference for the experimental design of basic research. Methods Eighteen 8-week-old SD male rats were randomly divided into sham, Minor CCI, and classic CCI groups with six animals in eachgroup. The 1-ligature was ligated on the sciatic nerve in the Minor CCI group, and the 4-ligature was ligated in the classicCCI group. Animals in the three groups were examined before modeling and at 7, 14, 21 and 28 days after modeling for themechanical withdrawal threshold, thermal withdrawal latency, and accumulated pain score. Ultrastructural changes of thesciatic nerve were observed by electron microscopy. Results Nociceptive symptoms of Minor and classic CCI groups were the same in terms of the mechanical withdrawal threshold and thermal withdrawal latency. Additionally, the accumulated pain score of the Minor CCI group was lower than that of the classic CCI group. Ultrastructural changes of the sciatic nerve in Minor and classic CCI groups were the same. Both of them showed destruction and disintegration of the myelin structure, formation of myelin spheres and autophagosomes. Conclusions The Minor CCI model is more stable and nociceptive symptoms can be maintained for up to 28 days after modeling, basically without self-mutilation, which is suitable for shortterm experimental design and minimizes the pain of experimental animals. The classic CCI model has long-lasting nociceptive symptoms that remain in the plateau period for 28 days after modeling, but the self-mutilation phenomenon is obvious, which is suitable for medium and long-term experimental designs.

Abstract:This study aimed at finding a common specific indication of tongue images between model rats and patients with Qi deficiency and blood stasis syndrome of CHD. Methods Images of tongues of patients with Qi deficiency and blood stasis syndrome of CHD were divided by mat lab software and relevant features were extracted. Whole clinical and animal samples were classified and identified using an RF model and the predictive value of the model was evaluated by the ROC. AUC was calculated to determine the diagnostic value of each index. Results Four indications named M1 , M2 , M3 and M5 were closely related to the diagnosis of CHD with Qi deficiency and blood stasis syndrome. In RF classification, FPR was 15. 2%, TPR was 83. 3%, the best boundary value was 0. 5, sensitivity was 81. 4%, specificity was 76%, accuracy was 85. 7%, circumferential convolution was 0. 6991, and AUC was 0. 8151. AUC indicated that all variables had diagnostic value, among which M1 , M2 and M5 had high diagnostic values and M3 had a moderate diagnostic value. In the rat model, significant differences in the characteristic values of M1 , M2 , M3 and M5 were observed compared with the normal group (P < 0. 05, P < 0. 01). In RF classification, FPR was 14. 8%, TPR was 83. 1%, AUC was 0. 8755, the best boundary value was 0. 5, sensitivity was 81. 8%, specificity was 75. 6%, accuracy was 83. 1%, and circumferential convolution was 0. 6451. AUC suggested that M1 , M2 , M3 and M5 had diagnostic value. Among them, M1 , M2 and M5 had high diagnostic values and M3 had a moderate diagnostic value. Conclusions The RF method can be used as a method of tongue image recognition in CHD with Qi deficiency and blood stasis syndrome. The characteristic values of M1 , M2 , M3 and M5 can be used as specific indications of clinical samples and animal models of CHD with Qi deficiency and blood stasis syndrome. The rat model of CHD Qi deficiency and blood stasis syndrome is in line with the digital characteristics of tongue diagnosis in patients.

Abstract:To investigate the protective effect and mechanism of the active ingredients in Huanglian Jiedu decoction in preventing brain nerve cell damage in a cell model of Parkinson’ s disease. Methods SH-SY5Y cells were divided into five groups: control group, model group, palmatine group, wogonin group and geniposide group. No substance was added to the cell culture medium of the control group, whereas 500 μmol / L of 1-methyl-4-phenylpyridinium ions (MPP+) was added to the other groups to create a cell model of Parkinson’ s disease. The palmatine group was supplemented with 10 μmol / L of palmatine, the wogonin group was supplemented with 50 μmol / L of wogonin, and the geniposide group was supplemented with 50 μmol / L of geniposide. The cell viability was detected by CCK-8, cell apoptosis was evaluated using Hoechst 33258 staining, and the expressions of α-synuclein (α-Syn) and tyrosine hydroxylase (TH) were detected by immunofluorescence. The concentrations of the tumor necrosis factor-α (TNF-α)、interferon-γ (IFN-γ)、interleukin-6 (IL-6) and interleukin-1β (IL-1β) were detected by enzyme-linked immunosorbent assay. The mRNA levels of the apoptosis-related proteins Bcl-2, Bax and Caspase-3 were detected by Real-time PCR. Results MPP+ stimulation significantly decreased the viability of SH-SY5Y cells; the α-synuclein fluorescence intensity was significantly increased,and the number of TH-positive cells was significantly decreased. Intervention with palmatine, wogonin and geniposide significantly increased the viability, decreased the α-synuclein fluorescence intensity, and increased the number of THpositive cells; furthermore, the concentrations of TNF-α, IFN-γ, IL-6 and IL-1β and the expression levels of Bax and Caspase-3 mRNA were significantly reduced, whereas the level of Bcl-2 mRNA was increased. Conclusions The active ingredients of Huanglian Jiedu decoction inhibit the release of inflammatory factors and thus inhibit the inflammatory response, providing a theoretical basis for the treatment of brain nerve cell injury in Parkinson’s disease.

Abstract:To investigate the feasibility and success rate of a rabbit model of acute pulmonary embolism by using a central venous catheter to measure pulmonary artery pressure and assessing the anatomical and pathological changes. Methods The central venous catheter was placed into the rabbit pulmonary artery through the internal jugular vein using a guidewire and was connected to the Medlab biological signal acquisition and processing system for dynamic pulmonary artery pressure monitoring. A model of acute pulmonary embolism with relatively consistent severity and embolization range was created by controlling the number of thrombi injected via the catheter to obtain the target pulmonary artery pressure. Results The modeling success rate was 100%. After embolization, there were significant changes in the pulmonary artery pressure, blood pressure, and heart rate of the rabbits ( P < 0. 05). Cardiopulmonary anatomic examination confirmed that the catheter was in the main pulmonary artery. Pathological examination revealed thrombi in the pulmonary artery and pulmonary arterioles. Conclusions A rabbit model of acute pulmonary embolism was established by inserting a central venous catheter through the jugular vein; this not only ensured the integrity of the thrombi, but also enabled the attainment of continuous and accurate pulmonary artery pressure data and effectively established an animal model with controllable embolization range and severity. This method has a high success rate, is technically simple and economical, and provides an experimental basis for the diagnosis and treatment of acute pulmonary embolism.

Abstract:To explore the feasibility of establishing a rat model of congenital abnormalities of the kidney and urinary tract (CAKUT) in offspring due to gestational diabetes mellitus (GDM). Methods Thirty naturally conceived SD rats were randomly divided into five groups by the concentration of streptozotocin (STZ) administered through a single intraperitoneal injection on day 1. 5 of gestation: 30 mg / kg STZ, 35 mg / kg STZ, 40 mg / kg STZ, solvent control (injected with the same dose of sodium citrate buffer), and blank control ( not injected with any liquid) group ( n = 6 in each group). Weight, blood glucose and abortion of pregnant rats were monitored during pregnancy. On the first day of delivery, the survival rates of offspring were calculated. Offspring were dissected and assessed for abnormalities of the urinary tract. HE staining of cross-sections of the offspring was performed, and renal and ureteral abnormalities were observed and recorded in multiple sections. Renal cortical thickness was measured in offspring. Results Ureteral dilatation and effusion (bilateral up to more than three times of unilateral) and renal dysplasia were observed in 30, 35 and 40 mg / kg STZ groups, and the total rates of ureteral effusion were >70%. HE staining revealed dilatation and effusion of the ureter, dysplasia of the ureteral wall, thinning of the renal parenchyma, and a reduction in the renal cortical thickness (more than 20% reduction compared with the blank control group). The blood glucose of all three groups reached the modeling standard, among which the mean blood glucose of the 30 mg / kg STZ group was lower than that of the 40 mg / kg STZ group (P<0. 05). Blood glucose in the 35 mg / kg STZ group was lower than that in the 40 mg / kg STZ group during early pregnancy (P<0. 05), and there was no difference during middle and late pregnancy (P>0. 05). Only pregnant rats in the 40 mg / kg STZ group aborted (33. 33% abortion rate), and survival rates in all three groups were lower than that in the blank control group (P<0. 05). Conclusions Establishment of a CAKUT model in offspring of GDM rats is feasible, and one intraperitoneal injection of 30 mg / kg STZ on day 1. 5 of gestation in SD rats safely and stably causes ureteral effusion (unilateral or bilateral) and renal dysplasia in offspring.

Abstract:To investigate the role of miR-146a / Sirt6 signaling-mediated autophagy in dexmedetomidine (DEX) treatment of intestinal ischemia-reperfusion ( I/ R) injury. Methods SD rats were randomly assigned to Sham, I/ R, and DEX groups with eight rats in each group. Except for the Sham group, the other groups underwent intestinal I/ R modeling. Rats in the DEX group were treated by an intraperitoneal injection of 25 μg / kg DEX at 30 min before ischemia. In vivo, intestinal histopathological examination and scoring were performed. In vitro experiments, the rat small intestinal crypt epithelial cell line IEC-6 was treated with DEX before deprivation / reoxygenation (OGD/ R) treatment. IEC-6 cell viability was analyzed by MTT assays. Apoptosis and miR-146a expression in intestines and IEC-6 cells were detected by TUNEL and quantitative real-time PCR, respectively. Sirt6 and LC3 expression in intestines and IEC-6 cells was detected by Western blot and immunofluorescence. Results Histopathological analysis indicated that DEX treatment protected against I/ R-induced intestinal epithelial damage and restored cell proliferation after OGD/ R exposure in a dose-dependent manner. Compared with the I/ R group, apoptosis in intestinal tissue of the DEX group was decreased significantly (P<0. 01), and of miR-146a, Sirt6 and LC3Ⅱ expression was increased significantly (P<0. 05). Consistent with the in vivo result, DEX significantly attenuated OGD/ R-induced apoptosis of IEC-6 cells (P<0. 01) and significantly increased the expression of miR-146a, Sirt6 and LC3Ⅱ in IEC-6 cells in vitro ( P < 0. 01). Furthermore, miR-146a inhibitor treatment of IEC-6 cells supported that miR-146a inhibition attenuated DEX-induced improvement and inhibited autophagy activation by downregulating Sirt6 expression. Conclusions DEX has a protective effect against I/ R injury by regulating miR-146a / Sirt6-mediated autophagy.

Abstract:To investigate the regulatory effect of miR-202-5p on proprotein convertase subtilisin / kexin type 9 (PCSK9) and its effect on neuronal damage in Alzheimer’s disease (AD). Methods SD rats were injected with amyloid β(Aβ) 1-42 into the lateral ventricle to establish an AD model and were randomly divided into normal control,model, ago-miR-202-5p, ago-NC and PCSK9 inhibitor groups. After the administration, spatial memory and learning ability tests were performed. Nissl staining was used to detect neuronal changes in cerebral cortex tissue. Neuron nuclear antigen (NeuN) immunofluorescence was used to detect the number of neurons in cerebral cortex tissue. ELISAs were used to measure the levels of PCSK9, β-amyloid 42 ( Aβ42 ), β-amyloid 40 ( Aβ40 ), and total cholesterol ( TC) in cerebrospinal fluid and tumor necrosis factor-α (TNF-α), interleukin-1β ( IL-1β), and phosphorylated Tau protein (Ptau) in cerebral cortex tissues. qRT-PCR was used to measure miR-202-5p expression in cerebral cortex tissue. Western blot was used to detect PCSK9, LDL receptor-related protein 1 (LRP-1), apolipoprotein E (ApoE), amyloid precursor protein (APP), and β site APP shearing enzyme 1 (BACE1) protein expression in cerebral cortex tissue. Dual luciferase assays were used to verify targeted regulation of PCSK9 by miR-202-5p. An in vitro AD cell model was established and cotransfected with miR-202-5p mimic and an PCSK9 overexpression vector ( pcDNA-PCSK9), and then reversal of the effect of PCSK9 overexpression on miR-202-5p was explored. Results Compared with the normal control group, the spatial memory and learning ability of rats in the model group were decreased, cerebral cortex neuron damage and number were decreased, PCSK9, Aβ42, Aβ40 and cholesterol levels in the cerebrospinal fluid were increased, P-tau and inflammatory factors levels in the cerebral cortex were increased, miR-202-5p expression was decreased, activity of the PCSK9 activation-mediated BACE1-APP-Aβ production pathway was increased, and LRP-1-ApoE-mediated promotion of cholesterol uptake and Aβ clearance activity were decreased (P<0. 05). miR-202-5p overexpression or PCSK9 inhibitor treatment suppressed neuronal damage caused by Aβ42 and Aβ40 deposition, reduced inflammatory factor secretion, inhibited BACE1, APP and Aβ production mediated by PCSK9 activation, and increased LRP-1-ApoE-mediated promotion of cholesterol uptake and Aβ clearance ( P < 0. 05). There was a targeted regulatory effect between miR-202-5p and PCSK9. Upregulation of PCSK9 partially attenuated the anti-AD effect of miR-202-5p overexpression ( P < 0. 05 ). Conclusions miR-202-5p overexpression inhibits Aβ production by suppressing PCSK9 activation and promoting LRP-1-ApoE-mediated cholesterol uptake and Aβ clearance, thereby exerting anti-AD nerve injury effect.

Abstract:To investigate the role of tumor necrosis factor α-induced protein 1 (TNFAIP1)-mediated RhoA ubiquitination in melanoma cell proliferation and invasion. Methods Bioinformatics analysis was performed to assess TNFAIP1 and RhoA expression in melanoma cell, followed by analyzing its expression in clinical tissues from melanoma patients. Gene and protein expression was assessed by RT-qPCR and Western blot assays, respectively. Human skin melanoma cell lines WM2664 and A2058 overexpressing TNFAIP1 and / or RhoA were established in vitro. Cell proliferation and invasion were investigated by colony formation, CCK-8 and Transwell assays. Plasmids expressing TNFAIP1 and RhoA were cotransfected into treated melanoma cells and immunoprecipitation assays were performed to determine the interaction between TNFAIP1 and RhoA. An in vivo model was established to confirm the effects of TNFAIP1 and RhoA on tumor growth and metastasis. Results Compared with adjacent normal tissues, TNFAIP1 expression was significantly decreased (P<0. 01) and RhoA expression was significantly increased (P<0. 01) in tumor tissues. Melanoma patients with high TNFAIP1 expression had a good prognosis, whereas melanoma patients with high RhoA expression had a poor prognosis. In vitro, TNFAIP1 overexpression significantly inhibited melanoma cell proliferation and invasion. TNFAIP1 mediated K48-linked ubiquitination of RhoA to promote its degradation. Rescue experiments showed that RhoA overexpression significantly inhibited the regulatory role of TNFAIP1 overexpression in melanin cell proliferation and invasion in vivo and in vitro. Conclusions TNFAIP1 has a tumor suppressor role in melanoma, which inhibits tumor cell proliferation and invasion by inducing RhoA ubiquitination.

Abstract:To study the effects of a high sucrose-high fat (HSHF) diet on growth and metabolism of inbred BALB/ c and C57BL/ 6J mice in parallel. Methods Litters of the two strains were weaned and separated by sex on day 25. Males and females of each strain were randomly divided into two groups. One group was fed a standard diet and other a HSHF diet from weaning until termination of the study ( 24 weeks). The parameters analyzed were the growth curve, levels of blood glucose and serum lipids, organ index ( spleen, liver and lungs), and histology of these organs. Results The strain determined the basal patterns of the growth curve, levels of blood glucose and serum low-density lipoprotein and triglycerides. Sex played a role in some of these parameters. The HSHF diet significantly altered the basal growth curve of females, but not males. In terms of metabolic parameters, the HSHF diet mostly increased their values. However, alterations of serum lipids were specific to the strain or sex. The severity of fatty changes in the liver varied with the strain and sex. Alterations of the spleen index depended significantly on the strain and sex. No histological changes were observed in the lungs. Conclusions Alterations of growth and metabolism caused by the HSHF diet were significantly influenced by the strain and sex. However, sex mainly modified differences determined by the strain.

Abstract:To examine the therapeutic effect of Kaixin San in rats with AD caused by bilateral Aβ1-42 injection into CA1 area of the hippocampus, and to preliminarily clarify its mechanisms. Methods Using the “β-amyloid protein toxicity theory”, the rat model of AD was established by bilaterally injecting Aβ1-42 oligopeptide segments in the CA1 region of the hippocampus of SD rats using a brain stereotaxic instrument. The rats were randomly divided into model, Hupezine A, Kaixin San low, middle and high dose groups, with 10 rats in each group. Another 10 rats were subjected to intracranial injection of an equal amount of physiological saline as the sham operation group and 10 normal rats were used as the blank control. The rats were subjected to continuous intragastric administrations for 30 days. Changes in learning and memory performance were observed by the Morris water maze behavioral test. HE and Nissl staining was used to visualize pathological morphology of the brain. The contents of cholinergic neurotransmitters ( ACh, AChE and ChAT ), proinflammatory factors (TNF-α, IL-6 and IL-1β), and β-amyloid protein (APP, Aβ1-40 and Aβ1-42 ) in brain tissue were measured by ELISA. Expression of tau protein and GSK-3β in cortical and hippocampal tissues was detected by IHC. BAX and BCL-2 expression in brain tissues was measured by Western blot. Results Compared with the model group, rats in the Kaixin San treatment groups had a significantly shorter escape latency, an increased number of platform crossings, and an enhanced dwell time and percentage of swimming distance to the total distance in the target quadrant (P<0. 05 or P<0. 01). The numbers of neurons in cortical and hippocampal tissues were increased, the morphological structure tended to be normalized, the number of Nissl bodies increased, and the cytoplasm darkened. AChE activity was attenuated, and ChAT with ACh levels were significantly increased in brain tissue (P<0. 05 or P<0. 01). TNF-α, IL-6, IL-1β, APP,Aβ1-40 and Aβ1-42 contents were decreased markedly (P<0. 05 or P<0. 01). Expression of tau protein and GSK-3β in both cortical and hippocampal tissues was downregulated (P<0. 05 or P<0. 01). BAX protein expression decreased, and the ratio of BCL-2/ BAX tended to increase to various degrees (P>0. 05). Conclusions Kaixin San has a good therapeutic effect on dementia symptoms and brain tissue damage in AD-injured rats, and its mechanisms involve the repair of the cholinergic system, inhibition of proinflammatory factor release, clearance of β-amyloid protein, and regulation of tau protein phosphorylation.

Abstract:To investigate the effect of matrine on endothelial injury and the Janus-activated kinase 2 / signal transducer and activator of transcription 3 / suppressor of cytokine signaling-1 ( JAK2 / STAT3 / SOSC1) signaling pathway in rats with pregnancy-induced hypertension (PIH). Methods Sixty pregnant rats were randomly separated into normal control group, model control group, low dose matrine group, high dose matrine group and magnesium sulfate group, with 12 rats in each group. Pregnant rats in each group except the normal control group were intragastrically administered 50 mg / kg nitroso-L-arginine methyl ester on day 12 of pregnancy to establish a PIH rat model. On day 16 of pregnancy, low and high dose matrine groups were administered intragastrically with 50 and 100 mg / kg matrine, respectively, the magnesium sulfate group was administered intragastrically with 100 mg / kg magnesium sulfate, and normal and model control groups were administered intragastrically with an equal volume of saline. A rat non-invasive sphygmomanometer and Coomassie blue staining were used to assess tail artery blood pressure and the 24 h urine protein content of pregnant rats in each group on day 16 (before administration), day 17 and day 21 of pregnancy. Enzyme-linked immunoassays were used to determine the levels of superoxide dismutase ( SOD), malondialdehyde ( MDA), tumor necrosis factor-α ( TNF-α), interleukin (IL)-6, IL-10, endothelin (ET), thromboxane B2 ( TXB2), nitric oxide (NO), and 6-keto-prostaglandin F1α ( 6-keto-PGF1α). Western blot was used to measure JAK2, p-JAK2, STAT3, p-STAT3 and SOSC1 protein expression in rat placental tissue. Results On the days 17 and 21 of pregnancy, blood pressure and the 24 h urine protein content of pregnant rats in the model control group were significantly higher than those in the normal control group (P< 0. 05), and blood pressure and the 24 h urine protein content of pregnant rats in low and high dose matrine groups were significantly lower than those in the model control group (P<0. 05). Compared with the normal control group, serum levels of SOD, IL-10, NO and 6-keto-PGF1α in the model control group were lower, and MDA, TNF-α, IL-6, ET and TXB2 levels and p-JAK2 / JAK2, p-STAT3 / STAT3 and SOSC1 protein expression in placental tissue were higher ( P< 0. 05). Compared with the model control group, SOD, IL-10, NO and 6-keto-PGF1α in low and high dose matrine groups were increased sequentially, and MDA, TNF-α, IL-6, ET and TXB2 levels and p-JAK2 / JAK2, p-STAT3 / STAT3, and SOSC1 protein expression in placental tissue were decreased sequentially (P<0. 05). Compared with the magnesium sulfate group, the above indicators in the high dose matrine group showed no significant changes ( P > 0. 05 ). ConclusionsMatrine decreases blood pressure, urinary protein content, inflammatory responses, and oxidative stress, inhibits JAK2 and STAT3 phosphorylation and SOSC1 protein expression, and then alleviates endothelial injury in PIH rats

Abstract:To investigate induction of endoplasmic reticulum stress-mediated apoptosis in diffuse large B-cell lymphoma cells by p-coumaric acid. Methods Diffuse large B-cell lymphoma cell line OCI-LY1 was treated with pcoumaric acid (0, 0. 4, 0. 8, 1. 6 and 3. 2 mmol / L) and the inhibition rate and half-inhibition concentration ( IC50 ) was determined by CCK8 assays. Subsequently, groupings were set as follows: (1) control group and p-coumaric acid groups (1 / 2 IC50 , IC50 and 2 IC50 ). (2) control group, p-coumaric acid IC50 group, 4-PBA group (5 mmol / L) and 4-PBA+IC50 group. Cell activity was assessed by CCK8 assays. Apoptosis was detected by flow cytometry. Relative expression of GRP78, ATF6, CHOP, p-PERK and p-IRE1α proteins was detected by Western blot. Results p-Coumaric acid inhibited OCI-LY1 cell proliferation in a dose-dependent manner with an IC50 value of 2. 601 mmol / L. Compared with the control group, the cell inhibition rate, apoptosis, and GRP78, ATF6, CHOP, p-PERK and p-IRE1α protein expression were significantly increased in the 1 / 2 IC50 , IC50 and 2 IC50 groups ( P < 0. 01). Compared with the IC50 group, the cell inhibition rate, apoptosis and GRP78, ATF6, CHOP, p-PERK, p-IRE1α protein expression were significantly decreased in the 4-PBA group and 4-PBA+IC50 group (P<0. 01). Compared with the 4-PBA group, cell inhibition rate, apoptosis and GRP78, ATF6, CHOP, p-PERK and p-IRE1α protein expression were significantly increased in the 4-PBA+ IC50 group (P<0. 01). Conclusions p-Coumaric acid inhibits OCI-LY1 cell proliferation, possibly by activating endoplasmic reticulum stress and inducing apoptosis.

Abstract:Henoch-Sch?nlein purpura (HSP) is a common systemic small vasculitis in childhood, which easily causes kidney damage. Compared with the large number of clinical studies on this disease, there are relatively few reports on animal models. Here, we systematically summarize the establishment, modeling method, advantages and disadvantages of the current domestic and foreign HSP animal models, expound the research status and existing problems of HSP animal models, and discuss and analyze the HSP animal model establishment to provide ideas and references for scientific research on this disease.

Abstract:As the main organ of human metabolism, the liver has important functions such as detoxification and bile secretion. Liver damage may lead to adverse consequences such as cirrhosis and liver failure. As the basis of liver disease research, liver injury has been widely subject to scientific research. Various chemicals are available to model liver injury with different pathogeneses. This review briefly introduces five mechanisms of animal liver injury caused by several chemical pathways, such as oxidative stress, interference of RNA synthesis, regulating enzyme activity, cholestasis induction, and promotion of tumor cell formation to provide ideas to study liver injury.

Abstract:Cardio-oncology is a new interdisciplinary subject involving oncology and cardiovascular disease. With the rapid development of tumor treatment strategies, the survival of patients has been prolonged, and the side effects of treatments, especially cardiovascular toxicity, have received increasing attention. The establishment of an animal model of cardio-oncology is helpful to understand the pathogenesis of cardiovascular toxicity and take cardioprotective measures to prevent irreversible damage. Currently, non-tumor-bearing rodents are used in experiments. They are widely used, but there are few studies on animal modeling method . In this review, animal models of cardio-oncology established by antitumor treatments, such as chemotherapy, molecular targeted therapy, and radiotherapy, in recent years were collected and sorted, and the advantages and disadvantages of various animal models and modeling method were summarized. This article reviews the aspects of the developing clinical cardio-oncology and provides insights for the development of clinical cardiooncology.

Abstract:Viral pneumonia is a highly infectious respiratory disease. The disease course develops rapidly and the incidence rate is increasing. Therefore, it is important to establish an animal model that corresponds to the clinical characteristics of traditional Chinese and Western medicines. This review summarizes the method, mechanisms and principles of the existing models by summarizing a large number of studies. In accordance with the proposed clinical diagnostic criteria of traditional Chinese and Western medicines, this study evaluated the anastomosis degree of traditional Chinese and Western medicines of various models. The result showed that the model of viral pneumonia with damp heat syndrome caused by a high fat diet, virus nasal drip, and swimming for 30 min had a high degree of clinical coincidence between traditional Chinese and Western medicines. The symptoms of fever, sore throat, cough, nasal congestion, runny nose, and dyspnea of the model animals are more consistent with the clinical characteristics of human viral pneumonia, and the pathological changes of lung tissue were obvious. There was a large number of inflammatory cells under the bronchial mucosa and around the tracheal wall, which was highly consistent with the damp heat syndrome type of viral pneumonia. By analyzing the advantages and disadvantages of each modeling method of viral pneumonia, this study provides suggestions on improving the animal model and ideas for in-depth study of the pathogenesis, diagnosis and treatment method to promote clinical research of viral pneumonia.

Abstract:Depression has become the most common mental illnesses. Its incidence is increasing yearly and the cause remains unclear. Therefore, it is urgent to explore the pathogenesis of depression and find treatments. In recent years with the continuous increase of research related to depression, intestinal flora have become a new research hotspot in the pathogenesis of depression. Intestinal flora directly and indirectly affect brain functions through various mechanisms and regulate behaviors such as stress, anxiety and depression. This review discusses the relationship between intestinal flora and studies of animal models and clinical depression, the possible regulatory mechanism of intestinal flora in the occurrence and development of depression, and the anti-depressant mechanism of probiotics to provide a new theoretical basis for the treatment of depression by intestinal flora.

Abstract:Currently, coronavirus disease 2019 (COVID-19), with its long hiding cycle and high infection rate, is spreading rapidly around the world and is seriously affecting people’s quality of life. There are a wide variety of antiviral drugs with different activity characteristics used for COVID patients; however, there is a lack of definitive evidence on the best clinical treatment for COVID-19, and the incidence of adverse reactions is relatively high. This article reviews the mechanisms of action, clinical application, usage and dosage, and monitoring of therapeutic drugs and the adverse reactions of small-molecule antiviral drugs, macromolecular biological drugs, traditional Chinese medicine, and other drugs for the treatment of coronary pneumonia. The information aims to provide a reference for rational drug use to treat coronary pneumonia.

Abstract:Psoriasis is a chronic inflammatory skin disease with a polygenic genetic background. Disorder of the immune system is the cause of the development and persistence of psoriasis inflammation. It is believed that overactivation of the IL-23 / Th17 axis is the main pathogenesis of psoriasis. Psoriasis is mainly characterized by erythema, scale, and infiltration, and some patients have recurrent attacks, which cause psychological and economic burdens to individuals. The 2018 edition of the Chinese guidelines for the diagnosis and treatment of psoriasis indicated that the basic syndrome types of psoriasis are blood-heat syndrome, blood stasis syndrome, blood dryness syndrome, heat-toxin syndrome, dampness-heat accumulation syndrome, and rheumatism obstruction syndrome. Clinical treatment needs to be based on the syndrome types of dialectical treatment. Therefore, the disease and syndrome of psoriasis combined with an animal model is an important basis to study traditional Chinese medicine in the treatment of psoriasis. There are many psoriasis models, but a combination of disease and syndrome animal model has not been established, which cannot fully and comprehensively reflect the performance of a traditional Chinese medicine syndrome. This review summarizes the existing disease-syndrome combination models to provide comprehensive basic support for the research of syndrome differentiation and treatment of psoriasis.

Abstract:Gastroesophageal reflux disease ( GERD) is a common disease in gastroenterology, and clinical manifestations are prone to recurrent attacks. It is considered a risk factor for the development of esophageal adenocarcinoma( EAC). Family studies have shown that GERD heritability is approximately 30%, COL3A1 and ABAT genes are significantly associated with genetic risk. Several genes, such as the IL-1 gene cluster, GNB3 and GSTP1, are strongly associated with the risk of GERD. Mutations in TP53 and single nucleotide polymorphisms of EGF, MMP, CCND1, CDX2 and COX-2 cause genomic instability and promote the development of Barrett’s esophagus and EAC in some individuals. This article reviews the role of molecular biology in the occurrence and development of GERD into EAC.