黄地安消胶囊抑制EndoMT干预糖尿病大血管病变的机制
Mechanism of Huangdi Anxiao (黄地安消)Capsules in Intervening T2DM Vascular Disease by EndoMT Inhibition
陶猛 1单莉 2张魏 1魏良兵 2高家荣2
作者信息
- 1. 安徽中医药大学第一附属医院,合肥 230031;安徽中医药大学药学院,合肥 230012
- 2. 安徽中医药大学第一附属医院,合肥 230031
- 折叠
摘要
目的:研究内皮细胞内皮间质转化(EndoMT)在糖尿病大血管病变过程中的影响及黄地安消胶囊的干预作用.方法:采用高脂高糖饲料联合链脲佐菌素(STZ)诱导复制糖尿病大鼠模型.并将成功建模的大鼠分为模型对照组、黄地安消胶囊3、6、12 g/kg组及二甲双胍0.72 g/kg组,分别给予相应药物干预6 w.观察各组大鼠一般情况,每周测定大鼠空腹血糖(FBG);观察大鼠胸主动脉组织的病理学特征;并检测转化生长因子β1(TGF-β1)、Smad2、Smad3蛋白及mRNA、α-平滑肌肌动蛋白(α-SMA)、血管内皮钙粘蛋白(VE-cadherin)蛋白表达.结果:与正常对照组比较,模型对照组大鼠体质量明显降低(P<0.05或P<0.01),空腹血糖(FBG)显著升高(P<0.01),胸主动脉血管中TGF-β1、Smad2、Smad3蛋白及mRNA表达显著上调(P<0.01),α-SMA蛋白表达显著上调,VE-cadherin蛋白表达显著下调(P<0.01),血管内皮病理损伤严重;与模型对照组比较,黄地安消胶囊各剂量组给药第10 w后,大鼠体质量明显升高(P<0.05或P<0.01),胸主动脉血管中TGF-β1、Smad2、Smad3蛋白及mRNA表达显著下调,α-SMA蛋白表达显著下调(P<0.01),VE-cadherin蛋白表达显著上调(P<0.01),大鼠胸主动脉病理损伤减轻.结论:黄地安消胶囊可抑制TGF-β/Smad通路改善内皮间质转化(EndoMT)所致大血管病变,减轻大鼠病理损伤.
Abstract
Objective:To investigate the effects of endothelial-to-mesenchymal transition (EndoMT) in the process of macrovascular lesions in dia-betic vascular disease and the intervention effect of Huangdi Anxiao (黄地安消) Capsules (HDAXC).Methods:The diabetic rat model was induced by high-fat and high-sugar diet combined with streptozotocin (STZ).The successfully modeled rats were divided into HDAXC groups (3,6,and 12 g/kg) and a metformin group (0.72 g/kg),and corresponding drugs were administered for 6 weeks.The general conditions of rats in each group were observed.Fasting blood glucose (FBG) was measured weekly.Pathological characteristics of thoracic aortic tissue were observed,and the expression levels of transforming growth factor β1 (TGF-β1),Smad2,Smad3 proteins and mRNA,α-smooth muscle actin (α-SMA),and vascular endothelial cadherin (VE-cadherin) proteins were detected.Results:Compared with the normal control group,the model group showed significant decrease in body weight (P<0.05 or P<0.01),significant increase in FBG (P<0.01),significant upreg-ulation of TGF-β1,Smad2,Smad3 proteins and mRNA in thoracic aortic blood vessels (P<0.01),significant upregulation of α-SMA protein expression (P<0.01),significant downregulation of VE-cadherin protein expression (P<0.01),and severe vascular endothelial pathology.Compared with the results in the model control group,after 10 weeks of treatment with HDAXC at various doses,the body weight of rats signifi-cantly increased (P<0.05 or P<0.01);the expression of TGF-β1,Smad2,Smad3 proteins and mRNA in thoracic aortic blood vessels were significantly downregulated;α-SMA protein expression was significantly downregulated (P<0.01);VE-cadherin protein expression was sig-nificantly upregulated (P<0.01);the pathological damage of thoracic aorta in rats was alleviated.Conclusion:HDAXC can inhibit the TGF-β/Smad pathway to improve macrovascular lesions caused by EndoMT,thereby reducing pathological damage in rats.
关键词
黄地安消胶囊/转化生长因子β1/Smad信号通路/内皮间质转化/糖尿病大血管病变Key words
Huangdi Anxiao (黄地安消) Capsules/Transforming growth factor β1/Smad pathway/Endothelial-to-mesenchymal transition/Diabetic vascular disease引用本文复制引用
出版年
2024
国家科技期刊平台
NSTL
万方数据