Effects of metformin on epithelial-mesenchymal transition of rat alveolar epithelial type II cells induced by TGF-β / 中国临床药理学与治疗学

AIM: To observe the effect of metformin (Met) on the endothelial-mesenchymal transition (EMT) of rat alveolar epithelial type II cells and its mechanism. METHODS: The RLE-6TN cells were divided into 6 groups as follows: Control group; transforming growth factor-β

Mast cell activation, TLR4-NF-κB/TNF-α pathway variation in rats' intestinal ischemia-reperfusion injury and Tongxinluo's therapeutic effect.

This study was designed to investigate mast cell activation and related TLR4-NF-κB/TNF-α pathway variation in 3 and 7 days' rats intestinal I/R injury, and TXL's intervention effect. Rat intestine I/R injury was carried out using superior mesenteric artery occlusion model with 30 min ischemia followed 3 or 7 days' reperfusion. Rats were administered TXL ultrafine power of 0.4, 0.8 and 1.6g/kg/d respectively for 3 or 7 days after modeling. Mast cell activation was determined by immunofluorescent double staining. TLR4, ANGPTL4 and microRNA126 were determined by RT-PCR. PECAM-1, NF-κB p65, TNF-α and VE-Cadherin were determined by immunohistochemical staining. Intestine I/R induced massively mast cell activation and overexpressed TLR4, NF-κB, TNF-α, PECAM-1, miR126 in 3 and 7 days. VE-cadherin and ANGPTL4 expression was reduced. TXL treatment attenuated mast cell activation and inhibited TLR4, NF-κB, TNF-α, PECAM-1 over-expression in 3 and 7 days, protected VE-cadherin and ANGPTL4 protein. Inflammation boomed in rats' intestine I/R injury for 3 and 7 days, characterized by mast cell and related TLR4-NF-κB/TNF-α pathway activation, accompanied with endothelial barrier dysfunction and enhanced vascular permeability. TXL treatment attenuated inflammation, protected endothelial barrier function. TXL treat intestine I/R injury, according with "Treat different diseases with the same method" in TCM theory.

Inhibition of PI3K/AKT signaling pathway by sesamin and vitamin E improves left ventricular fibrosis in spontaneously hypertensive rats / 中国临床药理学与治疗学

AIM: Sesamin (Ses) is one of the major lignans in sesame seeds with antihypertensive and antifibroticactivities, but its effect is weak. In this experiment, we combined vitamin E (VitE) and Ses to observe their effects on blood pressure and left ventricular fibrosis in spontaneously hypertensive rats (SHRs), and to explore its possible mechanism. METHODS: Male SHRs were randomly divided into SHRs+Ses+VitE group, SHRs+Ses group, SHRs+VitE group, and SHRs model group. Wistar-Kyoto (WKY) rats were setted as a normal control group. After 10 weeks of administration, systolic blood pressure (SBP) of rats was measured by tail cuff method, and the left ventricle was taken to calculate the organ index. Collagen deposition was observed by Masson staining, and cardiac collagen volume fraction (CVF) was analyzed. Expressions of collagen I, collagen III, transforming growth factor-β

DUOX2 mutations are frequently associated with congenital hypothyroidism in a Chinese Patients / 中华内分泌代谢杂志

Objective To investigate the prevalence of DUOX2 mutations in Chinese patients with congenital hypothyroidism (CH) and to discuss the inheritance pattern of DUOX2 gene.Methods Blood samples were collected from 91 CH children and their genomic DNA was extracted from peripheral blood leukocytes.All exons and exon-intron boundaries of DUOX2 were analyzed by target next-generation sequencing and family trios was established to study the inheritance pattern of DUOX2 gene.Results Fifty-four out of 91 children with CH carried DUOX2 mutation, with a prevalence of 59.34%.Of the 54 CH children, 36 carried DUOX2 biallelic mutations.In all 12 family trios with probands carrying biallelic DUOX2 mutations, the parents carried heterozygous DUOX2 mutations while still showing normal thyroid function, suggesting that CH caused by DUOX2 mutations is inherited in an autosomal recessive manner.Conclusion DUOX2 gene is one of the most frequently mutated genes in Chinese CH patients and its inheritance pattern is an autosomal recessive one.

Effects of sequoyitol on expression of NADPH oxidase subunits p22 phox and p47 phox in rats with type 2 diabetic liver disease / 药学学报

This study is to observe the effects of sequoyitol on the expression of NADPH oxidase subunits p22 phox and p47 phox in rats with type 2 diabetic liver diseases. The model of high fat and high sugar diet as well as intraperitoneal injection of small dose of streptozotocin (STZ, 35 mg x kg(-1)) induced diabetic rat liver disease was used. After sequoyitol (50, 25 and 12.5 mg x kg(-1)) was administrated for 6 weeks, the contents of blood glucose (BG), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total antioxidant capacity (T-AOC), hydrogen peroxide (H2O2), NO and insulin (Ins) were measured, liver p22 phox and p47 phox mRNA content was determined with real-time PCR and the expression of p22 phox and p47 phox protein was examined by Western blotting. In addition, pathological changes in liver were observed with HE staining. Sequoyitol could reduce the content of fasting blood glucose, ALT, AST, Ins and H2O2, restore insulin sensitive index (ISI) and weight, elevate liver tissue T-AOC and NO content, reduce the NADPH oxidase subunit liver tissue p22 phox and p47 phox mRNA and protein expression, as well as ameliorate liver pathologic lesions. The results showed that sequoyitol can ease the type 2 diabetic rat liver oxidative stress by lowering NADPH oxidase expression.