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该研究观察梓醇对2型糖尿病(T2DM)大鼠血管内皮功能的保护作用并探讨其抑制NADPH氧化酶表达的机制。40只高糖高脂饮食联合腹腔注射链脲佐菌素致糖尿病大鼠随机分为模型组、梓醇低、中、高剂量组(10,50,100 mg·kg-1·d-1)。另以10只健康Wistar大鼠作为正常组。正常组、模型组分别给予相当量的生理盐水。6周后全自动生化分析仪检测血糖、血脂;ELISA检测血清8-异前列腺素F2α(8-iso-PGF2α)含量;硝酸还原法检测血清一氧化氮(NO)水平;羟胺法检测血清超氧化物歧化酶(SOD)含量;观察离体胸主动脉环内皮依赖性血管舒张反应;荧光法检测主动脉组织活性氧(ROS)的水平;HE染色观察主动脉病理形态学改变;RT-PCR,western-blot分别检测主动脉组织Nox4,p22phox mRNA及蛋白表达。结果显示梓醇中、高剂量组血管内皮损伤明显减轻,主动脉ROS水平降低,血清NO水平升高,8-iso-PGF2α含量减少,SOD含量升高;主动脉组织Nox4,p22phox mRNA及蛋白表达均降低,差异均有统计学意义(P<0.05)。因此梓醇对T2DM血管内皮具有保护作用,其机制可能与其下调Nox4,p22phox表达,抑制氧化应激反应有关。
This study was to investigate the protective effect of catalpol on vascular endothelial function in type 2 diabetes mellitus (T2DM) rats and to explore its mechanism of inhibiting the expression of NADPH oxidase. Forty high glucose and high fat diets combined with streptozotocin-induced diabetic rats were randomly divided into model group and low, medium and high doses of catalpol (10, 50, 100 mg · kg-1 · d-1). Another 10 healthy Wistar rats as normal group. Normal group, model group were given a considerable amount of saline. Six weeks later, blood glucose and blood lipids were detected by automatic biochemical analyzer. The level of 8-iso-PGF2α in serum was detected by ELISA, the level of serum nitric oxide (NO) was measured by nitrate reduction, the level of serum superoxide dismutase Enzyme-linked immunosorbent assay (ELISA) was used to detect the endothelium-dependent vasorelaxation of isolated thoracic aorta rings. The levels of reactive oxygen species (ROS) in aorta tissue were detected by fluorometry. Pathological changes of aorta were observed by HE staining. blot were used to detect the expression of Nox4 and p22phox mRNA and protein in aortic tissue respectively. The results showed that catalpol medium and high dose group of vascular endothelial injury was significantly reduced, aortic ROS levels decreased, serum NO levels, 8-iso-PGF2α levels decreased, SOD increased; Aorta tissue Nox4, p22phox mRNA and protein expression All the differences were statistically significant (P <0.05). Therefore catalpol has a protective effect on T2DM vascular endothelial cells, the mechanism may be related to its down-regulation of Nox4, p22phox expression, inhibition of oxidative stress response.