实验性2型糖尿病大鼠心肌线粒体的氧自由基损伤

Oxygen free radical injury of myocardial mitochondria in the experimental type 2 diabetic rats

目的:研究糖尿病大鼠心肌线粒体氧自由基异常的机制。方法:测定正常对照组和链脲佐菌素(STZ)诱导的2型糖尿病大鼠心肌线粒体中一氧化氮(NO)、丙二醛(MDA)、细胞色素C(Cyt-C)和线粒体钙含量及超氧化物歧化酶(SOD)、一氧化氮合酶(NOS)活性,并用透射电镜观察病理学改变。结果:模型组心肌线粒体NO、NOS、MDA、钙和胞浆细胞色素C均显著高于对照组(P<0.05);线粒体细胞色素C和SOD均显著低于对照组(P<0.05)。电镜下,模型组肌原纤维排列紊乱,部分融解消失,线粒体肿胀变性,数目增多。结论:氧自由基异常及脂质过氧化作用参与糖尿病心肌的线粒体损伤;Cyt-C和线粒体钙的改变也是糖尿病心肌线粒体损伤的因素。

AIM ： To study the mechanism of diabetic cardiomyopathy and abnormality of oxygen free radicals. METHODS ： The contents of myocardial cytosolic cytochrome C, mitochondria cytochrome C, mitochondrial calcium, NO, MDA and the activity of SOD and NOS were determined in diabetic rats induced by STZ. The pathological changes were observed under transmission electron microscope. RESULTS： Compared to the normal and ganoderma group, the levels of mitochondrial NO, iNOS, MDA, calcium and plasma Cyt - C in rat myocardium were higher （ P 〈 0. 05 ） , while mitochondrial Cyt - C and SOD were lowered in model group （ P 〈 0. 05）. The bouncary indistinct, disorganization, a focal loss of muscular fibril, myocardium mitochondria swelling, pulmonary vascular endothelial cellular swelling and obstructed lumen of the capillary were also observed under transmission electronic microscope. CONCLUSION： The findings indicate that oxyradical and lipid peroxidation might be associated with the damage of myocardial mitochondria in NIDDM rats. Cyt - C and mitochondrial calcium is also involved in the process.