Abstract: Objective To evaluate the effects of vitallium metal, ZrO₂ ceramic and PMMA resin grinding dust on rat lung tissue. Methods The surface morphology and particle size distribution of three kinds of dental grinding dust were detected using a scanning electron microscope and laser particle size analyzer. Following exposure of established animal models to the above grinding dust, the total number of white blood cells and macrophages and the interleukin IL-6 and IL- 16 concentrations in bronchoalveolar lavage fluid were detected by Giemsa staining and enzyme-linked immunosorbent assay; HE staining was used to observe the pathological changes of lung tissue slices. Results Compared with the control group, the number of white blood cells and macrophages and the IL-6 and IL-16 concentrations in the dust-exposed groups were significantly increased, the infiltration of inflammatory cells was more obvious, and the lung tissue was structurally damaged and fibrotic. Compared with the non-finely ground group, the inflammatory cells and factors in the finely ground groups of vitallium metal and ZrO₂ ceramic were significantly increased. Conclusions Three kinds of dental grinding dusts can cause inflammatory injury and early fibrosis of rat lung tissue, and vitallium and ZrO₂ dusts after fine grinding exacerbate the inflammatory damage compared with the group of non-fine grinding.

Abstract: Objective To investigate the mechanism of Chaishao Liujun decoction on gastric mucosal cell proliferation and apoptosis in rats with chronic atrophic gastritis (CAG) of liver depression and spleen deficiency. Methods Twenty-six Sprague Dawley rats (male= 13) were randomly divided into normal (n= 6) and model groups (n= 20). CAG rat models of liver depression and spleen deficiency were established and evaluated by the compound factor modeling method. After modeling, they were randomly divided into CAG, vitamin (VI group), and Chaishao Liujun decoction (CS group) groups, with six rats in each group. The normal group was not treated. During the intervention process, the CS group was administered Chaishao Liujun decoction 5. 1 g / ( kg·d), the VI group was given vitamin suspension 240 mg / (kg·d), and the normal and CAG groups were given sterilized drinking water for 4 weeks. HE staining was used to observe pathological changes in the gastric mucosa. Quantitative real-time PCR was used to detect the expression of apoptosis genes c-myc and p53 and Immunohistochemistry was performed to detect PCNA and Ag-NOR. TdT-mediated dUTP nick end labeling staining was undertaken to detect the apoptosis index of the gastric mucosa. Results Compared with the normal group, the activity of the rats in the CAG group was decreased, and the pathological changes showed atrophy of the inherent glands in the gastric mucosa, infiltration of inflammatory cells, and increased expression of c-myc, p53, PCNA, Ag-NOR and the apoptosis index in the gastric mucosa (P< 0. 05 or P< 0. 01). Compared with the CAG group, the activity of rats increased, the pathological atrophy of gastric mucosa improved to a certain extent, and the infiltration of inflammatory cells decreased in the VI and CS groups. The expression of c-myc, p53, PCNA, Ag-NOR and the apoptosis index in the gastric mucosa of rats in CS group was decreased (P<0. 05 or P<0. 01), while the expression of c-myc and p53 in the gastric mucosa of rats in the VI group decreased (P< 0. 05 and P< 0. 01, respectively), and the expression of PCNA, Ag-NOR, and the apoptosis index was decreased, with no significant difference ( P> 0. 05 ). Compared with the VI group, the general condition and gastric mucosa morphology of the CS group were more significantly improved, c-myc and p53 mRNA expression was increased in the gastric mucosal, and the expression of PCNA and Ag- NOR and the apoptosis index were decreased, but the differences were not statistically significant (P>0. 05). Conclusions The proliferation and apoptosis of gastric mucosal cells are closely related to the development and evolution of CAG. Chaishao Liujun decoction has good therapeutic and repair effects on CAG rats with liver depression and spleen deficiency. The mechanism of action may be related to the inhibition of c-myc, p53, PCNA and Ag-NOR expression, regulating the excessive proliferation and apoptosis of gastric mucosal cells.

Abstract: Objective An animal model of 70% partial hepatectomy + liver dual arterial blood supply (LDABS) was established. Methods Seventy-six rats were divided into a training group (n= 40) and a model group (n= 36). In the model group, 70% partial hepatectomy (left lobe and middle lobe of liver) + double artery blood supply surgery of the liver was performed under a microscope. The general status of rats was observed after surgery, and the success and 1 week survival rates were calculated. Results Through simulated surgery in the training group, the learning curve was crossed. The surgery duration of the model group was (65. 3 ± 6. 56) min, and the vascular anastomosis time was (11. 1 ± 2. 53) min. During the surgery, there were no obvious side injuries and less bleeding, of no more than 0. 8 mL, was observed. One week later, the modeling success rate was 88. 9% ( 32 / 36), and the rats were in good condition. Conclusions Surgery consisting of 70% hepatectomy + LDABS in rats under a microscope is relatively complicated. However, after a period of microsurgery training, the improvements and innovation of the surgical mode, especially vascular anastomosis and perioperative nursing, resultsed in a high success rate and strong repeatability of the model, laying the foundation for further research on its application in liver regeneration, acute liver failure, and liver transplantation.

Abstract: Objective To explore the effects and toxicity of repeated administration of wall-removed Ganoderma lucidum spore powder for 6 weeks on the development of various systems in juvenile rats. Methods One hundred twenty- eight juvenile SD rats aged 24 days (postnatal day, PND24) were divided into vehicle control, low-dose, medium-dose and high-dose groups by the weight balance method . Each group was composed of 32 rats ( half male and half female), and received pure water or wall-removed Ganoderma lucidum spore powder 0. 8, 1. 8 and 4. 0 g / kg doses by gavage, respectively, each in a volume of 10 mL/ kg, once a day for 6 consecutive weeks (42 d). The day after drug withdrawal and 4 weeks after drug withdrawal, 10 / 16 and 6 / 16 rats in each group were necropsied, and routine toxicity indicators and indicators of growth and development, bone development, behavior, sex hormones, immune system development, and other indicators were detected. Results Each dose of wall-removed Ganoderma lucidum spore powder had no significant toxic effects on the clinical symptoms, weight, food intake, sexual development, behavior, hematology, serum biochemistry, ophthalmology, growth hormones, sex hormones, skeletal system development, immunology, histopathology, or other indicators of juvenile SD rats. However, the rats in the high-dose group had reversible abnormalities in some urine indicators ( all returned to normal after 4 weeks of drug withdrawal), which was considered to be related to the urine excretion of the test product components or their metabolites. In the water maze test of each dose group, the incubation period decreased, and the percentage of time in the target quadrant, as measured by space exploration, increased, suggesting that the learning and memory ability was enhanced, which may be related to its pharmacological effects. Conclusions Wall-removed Ganoderma lucidum spore powder has no obvious toxic effects in juvenile SD rats, and the NOAEL was 4. 0 g / kg.

Abstract: Objective To study the effect of fucosyltransferase 8 ( FUT8) expression on the proliferation and invasion ability of colorectal cancer cells, and to explore the molecular mechanism of its function. Methods The Gene Expression Profiling Interactive Analysis(GEPIA) database was used to analyze the expression levels of FUT8 in colorectal cancer tissues. SW480 colorectal cancer cells were routinely cultured and divided into a si-NC group and a si-FUT8 group that were transfected with NC siRNA and FUT8 siRNA, respectively. FUT8 knockdown was detected by Western blot.SW480 cells in the si-NC and si-FUT8 groups were treated with the AKT signaling activator SC79, and then divided into si- NC, si-FUT8, si-NC+SC79, and si-FUT8+SC79 groups. CCK8 and Boyden chamber assays were performed to detect the cell proliferation and invasion of each group. Western blot was used to detect the expression of AKT, pAKT, and β-catenin. Results The GEPIA database analysis showed that the expression of FUT8 in colorectal cancer tissue was significantly higher than that in normal colorectal tissue. Compared with the si-NC group, the expression of FUT8 in the cells of the si- FUT8 group was reduced ( P< 0. 05), while compared with the si-NC and si-NC + SC79 groups, the proliferation and invasion of si-FUT8 group and si-NC+SC79 group cells were reduced, and pAKT and β-catenin expression was decreased. The proliferation and invasion of the si-NC+SC79 group cells were increased compared with the si-FUT8 group, and pAKT and β-catenin expression was increased. Conclusions Knockdown of FUT8 may inhibit the proliferation and invasion of colorectal cancer cells by regulating the AKT/ β-catenin signaling pathway.

Abstract: Objective To investigate the role of autophagy in the improvement of myocardial ischemia-reperfusion injury in rats by Wushen-Shunmai capsule. Methods Following establishment of a myocardial ischemia-reperfusion injury model, rats were randomly divided into sham, model, Wushen-Shunmai capsule, and autophagy inhibitor ( Wushen- Shunmai capsule+LY294002) groups, with 15 rats in each group. The concentrations of serum cardiac troponin I ( cTnI) and creatine kinase isoenzyme MB ( CK-MB ) were detected by enzyme-linked immunosorbent assay ( ELISA ) . Myocardial infarction volume was measured by 2,3,5-triphenyltetrazolium chloride ( TTC) staining, and cardiomyocyte apoptosis was detected by terminal dexynucleotidyl transferase-mediated dUTP nick end labeling ( TUNEL) assay. The number of autophagy events was counted under electron microscope, while the expression of total PI3K, Akt, mammalian rapamycin target protein (mTOR) and its phosphorylated protein, and autophagy marker microtubule associated protein 1 light chain 3 ( LC3) was detected by Western blot. Results Compared with the sham group, serum cTnI, CK-MB concentration, myocardial infarction area ratio, apoptosis index, autophagy number, myocardial LC3-II/ LC3-I, caspase 3, and Bax were significantly higher in the model group ( P< 0. 05) , and the levels of p-PI3K/ PI3K, p-Akt / Akt, p- mTOR/ mTOR, and Bcl2 were significantly lower ( P< 0. 05) . Compared with the model group, serum cTnI, CK-MB concentration, myocardial infarction area ratio, apoptosis index, autophagy number, myocardial LC3-II/ LC3-I, caspase 3, and Bax were significantly lower in the Wushen-Shunmai capsule group (P<0. 05) , and the levels of p-PI3K/ PI3K, p-Akt / Akt, p-mTOR/ mTOR, and Bcl2 were significantly higher (P<0. 05) . Compared with the Wushen-Shunmai capsule group, serum cTnI, CK-MB concentration, myocardial infarction area ratio, apoptosis index, autophagy number, myocardial LC3-II/ LC3-I, caspase 3, and Bax were significantly higher in the autophagy inhibitor group (P<0. 05) , and the levels of p-PI3K/ PI3K, p-Akt / Akt, p-mTOR/ mTOR and Bcl2 were significantly lower (P<0. 05) . Conclusions Wushen-Shunmai capsule inhibits excessive autophagy of myocardial cells and plays a protective role in myocardial ischemia-reperfusion injury.

Abstract: Objective This study aimed to investigate the stereoscopic structure of the coronary artery in miniature pig heart and its application in preservation. Methods Five intact hearts from Guangxi Bama miniature pigs were selected as the experimental objects. Coronary artery casting specimens of the small pig hearts were made by perfusion and corrosion to explore the fabrication process of the small pig coronary artery casting model and three-dimensional ( 3D) model by using crystal-gutta percha embedding and 3D reconstruction technology. Results The result showed that,the model of small pig heart coronary artery cast embedding had high transparency,which could clearly observe the course and branch distribution of small pig heart coronary artery, and no cast branch was broken. The three-dimensional model constructs the anatomical structure of coronary artery in miniature pig heart, which has strong stereoscopic sense, no artifacts, and can be rotated and segmented at any angle in three-dimensional space. Conclusions The crystal embedded cast model can effectively protect the coronary artery cast specimens of miniature pigs, the 3D model can also provide a technical and empirical basis for 3D virtual simulation of animal models.

Abstract: Objective Research on the modeling points of constipation animal models to provide reference for improving the success rate of modeling. Methods Using “ secret” and “ animal models” as the subject terms, all experimental journal articles from January 2015 to July 2020 in the databases of China National Knowledge Infrastructure (CNKI), Wanfang, and Weipu were searched. Summarize the types of experimental animals, modeling methods, modeling methods, modeling time, testing indicators, etc., and conduct a summary analysis. Results One hundred forty-two journal articles that met the criteria were included. Sprague Dawley ( SD) rats and Kunming ( KM) mice were mainly used to replicate animal models of constipation. Compound diphenoxylate and loperamide were the most common method of modeling. The modeling time was mostly 7 d and 14 d, and the longest was slow transit constipation of 120 d. The index detection focused on the carbon ink advancement rate, defecation function, colon tissue immunohistochemistry, and serum biochemical indicators. Conclusions Existing animal models often use drug-induced single-factor modeling and lack a multi-factor modeling evaluation system. For example, the water-restricted food control method and the low-fiber diet method are more in line with the real pathogenic factors of constipation, but there are currently few related studies. At present, research on constipation models tends to evaluate test drugs by intestinal defecation function, colonic histopathological structure, and serum biochemical indicators. With the advancement of constipation research, brain-gut axis interactions provide new ideas for constipation research, and related experimental research can be explored in future constipation experiments.

Abstract: Objective To investigate the effect of metformin (Met) on airway inflammation in rats with chronic obstructive pulmonary disease ( COPD) by regulating microRNA ( miR) - 34a. Methods The COPD rat model was established by fumigation for 30 min daily for 30 d and instillation of 2 mL lipopolysaccharide (LPS) solution through the airway on days 1, 14 and 28. Quantitative Real-time PCR ( qRT-PCR) was performed to detect the effect of Met on the miR-34a level in lung tissue; white blood cell count in bronchoalveolar lavage fluid (BALF) and wright staining were used to detect the effect of Met; hematoxylin-eosin (HE) was used to detect the effect of Met on lung morphology; the serum interleukin IL-6, IL-8, IL-1β and tumor necrosis factor-α (TNF-α) levels were detected by enzyme-linked immunosorbent assay; Western blot was used to detect the effect of Met on the sirt1 protein level in lung tissue; TargetScan was applied to determine the 3′UTR and miR-34a binding sites of sirt1 mRNA, and was identified by the dual luciferase reporter gene detection kit. Results Compared with the control group, in the model group the sirt1 protein level and the proportion of monocytes to macrophages in lung tissue were decreased ( P< 0. 05) , whereas the miR-34a level, the number of white blood cells in BALF, the proportions of neutrophils, eosinophils and lymphocytes, and the serum IL-6, IL-8, IL-1β and TNF-α levels were increased ( P< 0. 05) . Met in the COPD animals alleviated the reduced sirt1 protein level in lung tissues, the reduced proportion of monocytes to macrophages, and the increased miR-34a levels, number of white blood cells in BALF, proportions of neutrophils, eosinophils and lymphocytes, and the serum IL-6, IL-8, IL-1β and TNF-α levels (P<0. 05) . An increase of the miR-34a level reversed the effect of Met on COPD rats. Dual luciferase verified that miR-34a and sirt1 had a targeting relationship. Conclusions Met down-regulated miR-34a and thereby up-regulated sirt1 to relieve airway inflammation in COPD, which provides an experimental basis for the potential clinical treatment of COPD with Met.

Abstract: Objective To determine the therapeutic effect of trigonelline in early pregnancy on rats with preeclampsia (PE) induced by the nitric oxide synthase antagonist N-nitro-1-arginine methyl ester (LNAME). Methods On day zero of pregnancy, 28 Sprague - Dawley rats were randomly assigned to four groups: pregnancy control group, LNAME-induced PE group, and prophylactic use of trigonelline small dose group and high-dose group. Blood pressure and proteinuria of the pregnant rats were measured, endothelial function of pregnant rats was evaluated by femoral artery ultrasound, and the expression of inflammatory factors and endothelial-related factors were detected by ELISA. Finally, the placenta and kidney of pregnant rats were harvested for immunohistochemical analysis and to analyze the status of inflammation-related pathways by Real-time fluorescent quantitative PCR and Western blot. Results Prophylactic administration of low-dose or high-dose trigonelline improved hypertension, proteinuria, and weight loss during pregnancy, fetal growth restriction and blood flow-mediated dilation caused by LNAME. Trigonelline may act through the IκBα/ NF-κB pathway, balance endothelium-related factors and reduce inflammation activation in placenta and kidney tissues. Conclusions The preventive use of trigonelline in a PE-like rat model induced by LNAME can reduce PE symptoms, promote fetal growth, protect endothelial function and reduce inflammation.

Abstract: Objective To study the mechanism of Guizhi Fuling Capsule treating in mammary gland hyperplasia by network pharmacology. Methods Using PharmMapper, GeneCards, PubMed, GenCLip 3, and STRING platform to screen mammary gland hyperplasia targets of constituents migrating to blood, we constructed a protein-protein interaction (PPI) network. These targets were imported into the CytoNCA plug-in to calculate the important topological parameters of the PPI network to screen key targets. The ClueGO plug-in was used to analyze the biological process of these key targets, and the DAVID database was used to analyze KEGG pathway enrichment. Results Twelve constituents of constituents migrating to blood of Guizhi Fuling Capsule acted on 197 targets in mammary gland hyperplasia, which included 31 key targets, such as transcriptional and apoptotic proteins AKT1, MAPK1, CASP3, MAPK8, BCL2L1, MDM2, and STAT1, signal transduction proteins SRC, HRAS, HSP90AA1, MAPK14, PIK3R1, MAP2K1, and PTPN11, angiogenesis-related targets EGFR, MMP2, KDR, and NOS3, hormone-related receptors IGF1, ESR1, AR, and IGF1R, inflammatory factor IL2, and oxidoreductase CAT. These targets were enriched in 14 different biological processes, including inositol lipid- mediated signaling, mammary gland epithelium development, cellular response to reactive oxygen species, positive regulation of nitric-oxide synthase biosynthesis, T cell co-stimulation, and VEGF receptor signaling pathway, and regulate signaling pathways such as estrogen, prolactin, apoptosis, PI3K-Akt, VEGF, T cell receptors, TNF, and MAPK. Conclusions Guizhi Fuling Capsule is mainly used for the treatment of mammary gland hyperplasia by restoring the balance of sex hormones and promoting the apoptosis of mammary gland cells, as well as having anti-inflammatory, anti- oxidation, anti-angiogenesis, and other pharmacological effects.

Abstract: Objective The ginsenosides, polysaccharides and adenosine contents in the Dendrobium-ginseng- paecilomyces batmoth-ginger Capsule were determined. To study the immune function effect of Dendrobium-ginseng- paecilomyces batmoth-ginger Capsule in CI/ F1 (BALB/ c×ICR) female mice. Methods Ginsenoside and polysaccharide were determined by colorimetric method and adenosine was determined by High Performance Liquid Chromatography (HPLC). Dendrobium-ginseng-paecilomyces batmoth-ginger Capsule in distilled water was administered by oral gavage to female mice at a dose of 260, 530 or 1580 mg / kg. After 30 d, the bodyweight, immune organ index, spleen lymphocyte proliferation ability, delayed type hypersensitivity, serum hemolysin, natural killer (NK) cell activity, antibody generation cellular level and the changes of macrophage phagocytic function in the abdominal cavity were evaluated for 10 female animals in each group at the end of the study. Results The ginsenoside, polysaccharide and adenosine contents in Dendrobium-ginseng-paecilomyces batmoth-ginger Capsule were 1. 495 g / 100 g, 12. 90 g / 100 g and 73. 8 mg / 100 g, respectively. In the 1580 mg / kg group, the cellular immune function ( spleen lymphocyte proliferation and delayed type hypersensitivity reaction) in the mice were enhanced, the level of antibody generation was elevated and the macrophage cellular and phagocytic activities were increased. Conclusions Under the conditions of this experiment, the Dendrobium- ginseng-paecilomyces batmoth-ginger Capsule enhanced the immune function in mice.

Abstract: Objective To investigate the effect of piceatannol (PIC) on rat brain damage caused by acute carbon monoxide (CO) poisoning through the mitogen-activated protein kinase / extracellular siganl-regulated kinase(MAPK/ ERK) pathway. Methods SPF male SD rats was randomly assigned to four groups( 25 rats each group). Three groups were infused with CO gas for 1 hour to establish an acute CO poisoning model. The negative control (NC) group did not receive any CO. Following removal from the CO, the percent of carboxygenhemoglobin(HbCO%) of the rats in all four groups was determined immediately. Subsequently, the PIC group received 2 mL 200 mg / kg PIC by intragastric administration, the PIC + ERK group was similarly treated with both 2 mL 200 mg / kg PIC and 0. 2 mg / kg ERK inhibitor P-4313, and the CO and NC groups were treated with an equal volume of normal saline. A water maze experiment was performed after 1, 7, 14, 21 and 28 d. After completing this experiment, the brain tissues of all the animals were obtained for hematoxylin-eosin (HE) staining observation, Terminal deoxynucleotidyl transferase-mediated dUTP Nick-End labeling(TUNEL) staining to detect cell apoptosis, ultrastructure observation of neurons in brain tissue, detection of mitochondrial membrane potential, detection of the oxidative stress damage index of brain tissue cells, and Western blot detection of the nuclear factor E2 related factor 2(Nrf-2) and B-cell lymphoma-2(Bcl-2) proteins. Results In comparison with the NC group, rats in the CO and PIC + ERK groups displayed poorer learning and memory performance in the water maze experiment, the brain tissue cell morphology was changed, the ultrastructure of nerve cells was disrupted, the number of apoptotic cells was greater (P< 0.001), the mean fluorescence intensity(MFI) value was significantly decreased ( P< 0. 001) and the reactive oxygen species(ROS) content was elevated (P<0. 001). In contrast with the CO group, rats in the PIC group were normal in the behavioral experiments and the brain tissue cell morphology did not change; furthermore, fewer apoptotic cells were found (P<0. 001), the ultrastructure of nerve cells was intact, the MFI value and ROS content were lower (P<0. 001), and the Nrf-2 and Bcl-2 protein expression were slightly increased. Conclusions PIC may increase Nrf-2 and Bcl-2 expression through the MAPK/ ERK signaling pathway to protect against brain damage caused by acute carbon monoxide poisoning.

Abstract: Objective To investigate the effects of oxidative stress on human uterine ligament fibroblast proliferation, apoptosis, collagen synthesis and expression of inflammatory factors. Methods Third generation rat uterine ligament fibroblasts were divided into low oxidative stress, high oxidative stress and control groups. Hydrogen peroxide at 0. 2 mmol / L and 0. 8 mmol / L was applied to uterine ligament fibroblasts for 4 h to establish low and high level oxidative stress models, respectively. The methyl thiazolyl tetrazolium(MTT) assay was used to detect cell proliferation, the Annexin V-fluorescein isothiocyanate / propidium iodide(V-FITC/ PI) method was applied to detect apoptosis, and Western blot was used to detect the protein levels of type I collagen, type III collagen, inflammatory factors and signal pathway-related proteins. Results Compared with the control and low oxidative stress groups, the proliferation ability of cells in the high oxidative stress group was decreased (P<0. 05), the apoptosis rate was increased (P<0. 05), the synthesis of type I and type III collagen was decreased (P<0. 05), and the protein expression levels of interleukin ( IL) -1β, tumour necrosis factor alpha(TNF-α) and IL-6 were increased (P< 0.05). Compared with the control and low oxidative stress groups, phosphorylated-extracellular signal-regulated kinase 1 / 2(ERK1 / 2) and phosphorylated- protein kinase B(Akt) expression in the high oxidative stress group was decreased (P< 0. 05), whereas the expression of total protein ERK1 / 2 and Akt remained almost unchanged. There were no significant difference between the low oxidative stress and control groups. Conclusions A high hydrogen peroxide concentration in an oxidative stress microenvironment can inhibit ERK1 / 2 expression in the MAPK pathway and Akt expression in the phosphoinositide 3-kinase(PI3K) / Akt pathway, resultsing in decreased uterine ligament fibroblast proliferation and collagen synthesis and increased expression of apoptotic cells and inflammatory factors, which may participate in the occurrence and development of pelvic organ prolapse.

Abstract: Objective To investigate whether the vascular endothelial growth factor-A (VEGF-A) inhibitor sFLT- 1(soluble fms-like tyrosin kinase-1)can reverse renal dysfunction in type 1 diabetic mice by inhibiting vascular endothelial cell activation and inflammation. Methods Twenty-five eight-week-old C57BL/ 6 female mice were divided into two groups:two groups treated for 5 weeks: healthy control group (n= 5) and diabetic group (n= 5), and three groups for 15 weeks: healthy control group (n= 5), diabetic group (n= 5), control+sFLT-1 treatment group (n= 5), diabetic+ sFLT-1 treatment group (n= 5). The model of type 1 diabetes was established by intraperitoneal streptozotocin (75 mg / kg) injection. The treated mice received sFLT-1 at the sixth week after the establishment of the model. Renal pathological damage, macrophage infiltration, glomerular endothelial cell activation and inflammation were observed before and after sFLT-1 treatment. Results Compared with the model group, sFLT-1 transfection significantly reduced the content of the glomerular mesangial matrix (glomerular type IV collagen) (P< 0.001), glomerular macrophage infiltration (P< 0.001), glomerular endothelial cell activation (P< 0.001) and the glomerular tumor necrosis factor-α level (P< 0. 001), and thus significantly inhibited diabetic renal injury. Additionally, sFLT-1 reduced the activation of endothelial cells induced by VEGF-A in vitro (P< 0.001). Conclusions sFLT-1 may reduce endothelial activation and glomerular inflammation by inhibiting VEGF-A, and finally reverse diabetes-related renal damage, which is a new direction of treatment for diabetic nephropathy.

Abstract: Objective To establish a simple reliable and accurately method of non-invasive intratracheal intubation in mice. Methods Female C57BL/ 6 mice were used. Mice were anesthetized with pentobarbital sodium, then suspended via the upper incisors using surgical thread. An epidural anesthesia catheter, 1 mL syringe, 10 μL pipet tip, were assembled as intratracheal intubation equipment. Using the non-dominant hand to feel the trachea, the dominant hand inserted the equipment into the mouth cavity to deliver the liquid. The mice were administered trypan blue or PBS. After intratracheal intubation, mice that received trypan blue were killed and the lungs were checked, while the mice that received PBS remained under observation for monitoring of survival. Results The lungs of mice that received trypan blue were dyed blue, while the stomach was not dyed. The mice that received PBS remained alive after recovering from the anesthesia. Conclusions Equipment comprising an epidural anesthesia catheter, a 1 mL syringe, a 10 μL pipet tip, and ophthalmic forceps enable simple and accurate non-invasive intratracheal intubation.

Abstract:Gastric cancer is one of the most serious malignant tumors worldwide, and metastasis is the main cause of its high mortality. The identification of genes related to gastric cancer metastasis could help to understand the developmental mechanism of gastric cancer, which will provide a foundation for the prevention and targeted therapy of gastric cancer. In this paper, we review the latest research progress in the use of animal models to screen gastric cancer metastasis-related genes and to study gene function identification method. We focus on the characteristics of different metastasis models and the method for evaluating metastasis-related gene function in vitro and in vivo. This review aims to present the ideal experimental tools for the study of the mechanism of gastric cancer metastasis and the screening of new therapeutic targets.

Abstract:Muscle atrophy is the most common complication in cancer cachexia patients, resultsing in a serious prognosis. Various drugs for muscle atrophy have effects on the remission of cancer cachexia. Among them, the regulatory role of JAK/ STAT3 has attracted attention. In recent years, the mechanism of JAK/ STAT3 signaling regulating sarcopenia in cancer cachexia and related drug intervention has been studied in basic research and clinical experiments. These studies concluded that the JAK/ STAT3 signaling pathway can regulate muscle atrophy in cancer cachexia through the ubiquitin proteasome system, the autophagy lysosome system, microRNA and the tumor microenvironment. Specific drugs can effectively alleviate the process of cancer cachexia muscle atrophy by interfering with the JAK/ STAT3 signaling pathway.

Abstract:Allergic diseases are prevalent and they continue to affect human health. It is urgent to explore their pathogenesis and effective treatment method . In this process of exploration, the establishment of allergic disease models is a key factor. According to the classification of allergic diseases in different systems of the body, this article summarizes and analyzes the existing in vivo and in vitro models of allergic diseases, and compares the similarities, differences, advantages and disadvantages among them, aiming to provide information for the development and application of allergic disease models.

Abstract:BORIS (brother of the regulator of imprinted sites) was first expressed in amniotes during the evolution of vertebrates. Under human physiological conditions, this protein is highly expressed in male testes only. The expression sequence of BORIS in male mice is highly consistent with the sequence of spermatogenesis. Male BORIS knockout mice are sterile, while females are normal. BORIS induces the expression of specific genes in germ cells and has an important role in spermatogenesis, specifically regulating spermatogenesis under normal physiological conditions. Referring to recent studies of BORIS transgenic mice, BORIS knockout mice, and BORIS expression in testis, this review summarizes the expression and localization of BORIS in testis, the mechanism of BORIS in spermatogenesis, and the functional research and drug screening of BORIS, providing a new reference for molecular targeted therapy.

Abstract:Esophageal cancer is globally one of the most common malignant tumors of the digestive tract. Its morbidity and mortality are increasing annually, and it tends to affect more young people. The pathogenesis, metastasis, and drug resistance mechanisms of esophageal cancer are not fully understood. The anti-tumor role and reversal of drug resistance by traditional Chinese medicine have received increasing attention. The mouse model of esophageal cancer is helpful to analyze the pathogenesis of human esophageal cancer and the research strategy of traditional Chinese medicine on tumor prevention. Mouse models of esophageal cancer are mainly divided into three categories, induced models, transplanted models, and genetically engineered models. However, no model can represent all the characteristics of human esophageal cancer. It is particularly important to choose a suitable mouse model of esophageal cancer to solve specific esophageal cancer problems. This article summarizes the domestic and international research literature, reviews the current commonly used mouse esophageal cancer models, summarizes the preparation method of various types of esophageal cancer mouse models, and compares the advantages and disadvantages of each model and the scope of application, to provide a research basis for the prevention and treatment of esophageal cancer by traditional Chinese medicine.

Abstract:The protein tyrosine phosphorylation signal pathways are important signal transduction pathways, which are widely present in cells. Their function is closely related to cell proliferation, differentiation, transformation and apoptosis. Alzheimer’s disease (AD) is a degenerative disease of the nervous system. Age is the greatest risk factor for AD, and the likelihood of suffering from AD is age dependent. The main pathological features are the aggregation of β- amyloid protein and abnormal phosphorylation of Tau protein. The treatment of AD with tyrosine kinase inhibitors has become a greatly discussed topic in modern medical research. Therefore, the basic research progress of the relationship between the protein tyrosine phosphorylation signaling pathways and AD is briefly reviewed in this paper.