替米沙坦对2型糖尿病大鼠心肌保护作用及机制

目的探讨替米沙坦对2型糖尿病大鼠心肌的保护作用及细胞因子机制。方法30只雄性SD大鼠随机分为三组：正常对照组（C组）10只,糖尿病模型组（D组）10只,替米沙坦组（T组）10只,各组大鼠均在12周末结束实验。免疫组化方法检测心肌组织中TGF-β1,HGF蛋白及Ⅰ型胶原和Ⅲ型胶原表达。电镜观察左室心肌。结果与C组比较,D组心肌细胞内线粒体数目增多,肌原纤维灶性变性、溶解,肌原纤维间间隙增宽。与D组相比,T组心肌细胞内线粒体数目减少,肌原纤维灶性变性、溶解减轻。与C组比较,D组,T组TGF-β1,HGF,CollagenI和CollagenⅢ表达均显著升高（P〈0.01）。与D组相比,T组TGF-β1,CollagenI和CollagenⅢ表达均低于D组（P〈0.05）;T组HGF蛋白表达显著高于D组（P〈0.01）。结论替米沙坦能够改善糖尿病大鼠心肌超微结构,可能与降低心肌中TGF-β1蛋白,升高HGF蛋白表达有关。

Effects of Telmisartan on Ultrastructure of Myocardium in Diabetic Rats

Objective To explore the protection of myocardia by telmisartan and the effects of cytokines in diabetic rats＇ eardiomyopathy. Methods 30 male SD rats were randomly divided into three groups： the normal control group （group C）, diabetes control group（ group D）, telmisartan intervention group（ group T）. The experiment ended 12 weeks after giving telmisartan. Left ventricular tissue was processed for morpho- logical examination with electron microscope. The expressions of TGF-β1 and HGF protein and collagen Ⅰ and collagen Ⅲ were determined by immunohistochemistry method. Results Myocardium of group D was characterized by the increase of mitochondria compared with group C, and the interval of myofibril enlarged. However, myocardial pathological changes in group T was compared with group D. The levels of TGF-β1, HGF, col- lagen Ⅰ and collagenⅢ of groups D and T were increased significantly compared wiht group C. （P 〈0.01）. The levels of TGF-βt, collagen Ⅰ and collagen Ⅲof group T were declined statistically compared with group D （ P 〈 0.05）. The levels of HGF of group T were increased statistically compared with group D（ P 〈 0. 01 ）. Conclusion Telmisartan can improve ultrastructure of myocardium of diabetic rats and its protective effect may be related to the reduction of TGF-β1 and increase of HGF.