摘要
目的:探讨瑞苏伐他汀对2型糖尿病大鼠心肌病变的防治作用及其作用机制.方法:STZ注射诱导制备T2DM大鼠模型,成功模型随机分为对照组(B组,n=25)、瑞苏伐他汀组(C组,n=25),并设正常对照组(A组,n=10).于第14周末取大鼠心脏,称取心脏质量并计算心脏肥厚指数(HWI),胶原容积分数(CVF),电镜观察心肌超微结构;应用免疫组化法检测过氧化物酶体激活物受体α(PPARα)在心肌组织中的表达.结果:B组大鼠表现出心肌病特征,HWI,CVF增加,电镜观察可见大鼠心肌纤维以变性坏死为主,肌丝纤维丢失,肌丝排列紊乱,间质胶原纤维增多,糖原、脂褐素沉积等病理改变,C组大鼠心肌病变较B组有所减轻,HWI,CVF下降,免疫组化图像分析显示,B组大鼠心肌PPARa蛋白表达比A组明显升高,C组大鼠PPARα蛋白表达比B组明显升高,差别均具有统计学意义(均P<0.01).结论:瑞苏伐他汀在调脂的基础上,通过提高心肌PPARα的表达,对T2DM的心肌病变具有保护作用.
Abstract
AIM:To study the protective effects and the mechanism of Rosuvastatin on type 2 diabetic rats.METHODS:Type 2 diabetes meUitus(T2DM)rat model wag copied by giving SD rats a low dose of STZ.T2DM rats were divided randomly into control group(group B,n=25),Rosuvastatin group(group C,n=25),normal group was build(group A,n=10).At the end of 14 weeks,the HWI,CVF were detected,ultrastruetttre of left ventricle were observed with electron microscopes.The protein expression of PPARct in myocardium was detected by immunohistochemical staining.RESULTS:In group B,DCM hearts demonstrated diabetic cardiomyopathy phenotype,HWI and CVF were higher than that in group A,cardiac muscle degeneration,focal necrosis and region adipocytes infiltrating could be observed.Foregoing changes in group C rats were more relieved than those in group B rats.The protein expression of PPARα in myocardium showed that the IDP of PPARct in group B was higher than in group A rats and the IDP in group C rats was higher than that in group B rats(P<0.01).CONCLUSION:Rosuvastatin based on TC lowering,elicits benefitial effects on cardiovascular diseases by increasing PPARα expression.
NETL
NSTL
维普
万方数据