糖尿病大鼠心肌超微结构改变及过氧化物酶体增殖激活受体gamma配体对其作用的研究

Protective effect of rosiglitazone on myocardium in diabetic cardiomyopathy of rats

目的:明确糖尿病大鼠心肌超微结构改变及过氧化物酶体增殖激活受体(PPAR)gamm a配体(罗格列酮)对之的作用。方法:建立6周和10周糖尿病大鼠组,其中10周糖尿病大鼠的1组用PPARgamm a配体治疗,各组左心室心肌制作透射电镜标本。结果:STZ诱导的糖尿病大鼠心肌细胞胞浆肌原纤维束减少并断裂、融合,肌原纤维束与线粒体结构排列紊乱,线粒体崩解,细胞核固缩,核仁消失。10周组糖尿病大鼠心肌超微结构破坏比6周组明显。与未治疗组比,罗格列酮治疗组心肌结构完整、清晰,基本和正常大鼠心肌超微结构相似。结论:高血糖引起心肌超微结构损伤明显,糖尿病病程越长病变越明显;PPARgamm a配体具有心肌保护作用,而且不依赖于降血糖。

Objective： To investigate the protective effect of PPARgamma ligands rosiglitazone on myocardium in diabetic cardiomyopathy of rats. Methods： The rat model of diabetes was induced by administration of streptozotocin （STZ） for 6 or 10 weeks. In the treatment group the STZ-induced diabetic rats were treated with rosiglitazone. The left ventricular muscle specimens were taken from treatment and control group; then were examined under transmission electron microscope. Results： Cardiac myofibrils of diabetic rats in control group were obviously fewer and broken. There were fewer and smaller dissolved mitochondria with incomplete membrane and mixed cristae and karyopyknosis. Myocardium of diabetic rats treated with rosiglitazone was markedly improved although their blood glucose levels were still high. Conclusions： Hyperglycemia can cause destruction of myocardial cell structure. Rosiglitazone has protective effect on myocardial cells of diabetic rats ,which seems to be independent of blood glucose levels.