title: [Effect of sequoyitol on expression of NOX4 and eNOS in aortas of type 2 diabetic rats].
abstract: The aim of the present study is to investigate the effects of sequoyitol (Seq) on expression of eNOS and NOX4 in aortas of type 2 diabetic rats. Type 2 diabetic rats induced by high fat and high sugar diet and low dose of streptozotocin (STZ, 35 mg x kg(-1)) and were administered Seq (12.5, 25 and 50 mg x kg(-1) x d(-1)) for 6 weeks. The fasting blood glucose (FBG) and body weight were tested. Acetylcholine (Ach) induced endothelium-dependent relaxation and sodium nitroprusside (SNP) induced endothelium-independent relaxation were measured in aortas for estimating endothelial function. Aortic morphological change was observed with HE staining. The level of serum insulin was measured by radioimmunoassay. The total antioxidative capacity (T-AOC), malondialdehyde (MDA) and NO levels in aortas were determined according to the manufacturer's instructions. In addition, the expressions of eNOS and NOX4 in aortas were measured by immunohistochemisty, real-time PCR or Western blotting. The results showed that Seq significantly decreased FBG and insulin resistance, and improved aortic endothelium-dependent vasorelaxation function. The expressions of NOX4 and MDA content were obviously decreased, while the expression of eNOS, the levels of NO and T-AOC increased significantly in aortas of diabetic rats with Seq treatment. In conclusion, Seq protects against aortic endothelial dysfunction of type 2 diabetic rats through down-regulating expression of NOX4 and up-regulating eNOS expression.
authors: Xian-Wei
authors: XW
authors: Li
authors: Wei
authors: W
authors: Hao
authors: Yan
authors: Y
authors: Liu
authors: Jie-Ren
authors: JR
authors: Yang
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism* / Q000473:pathology; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D003924:Diabetes Mellitus, Type 2 / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D007004:Hypoglycemic Agents / Q000494:pharmacology; D007294:Inositol / Q000031:analogs & derivatives* / Q000494:pharmacology; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D000074663:NADPH Oxidase 4; D019255:NADPH Oxidases / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D010084:Oxidation-Reduction / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013311:Streptozocin; D014664:Vasodilation / Q000187:drug effects
chemical_list: C572459:5-O-methyl-myo-inositol; D001786:Blood Glucose; D007004:Hypoglycemic Agents; D007328:Insulin; D009569:Nitric Oxide; D007294:Inositol; D008315:Malondialdehyde; D013311:Streptozocin; D052250:Nitric Oxide Synthase Type III; C496316:Nos3 protein, rat; D000074663:NADPH Oxidase 4; D019255:NADPH Oxidases; C498911:Nox4 protein, rat