L-精氨酸对糖尿病大鼠肝、心肌及膈肌线粒体自由基损伤的保护作用

目的探讨L-精氨酸(L-Arg)对糖尿病大鼠肝脏、心肌及膈肌线粒体自由基损伤的保护作用. 方法给大鼠腹腔注射四氧嘧啶制备糖尿病模型,随机分为糖尿病组、L-Arg治疗组及正常对照组;用药4 w末测定三组大鼠肝脏、心肌及膈肌细胞线粒体中Mn-SOD、GSH-Px活性和MDA含量及膈肌线粒体内GSH含量.结果糖尿病组较正常组,大鼠肝、心肌、膈肌线粒体内GSH-Px活性显著降低(P＜0.01,P＜0.05,P＜0.001),MDA含量显著升高(P＜0.01,P＜0.05,P＜0.01),肝、膈肌线粒体Mn-SOD活性(均P＜0.01)及膈肌线粒体GSH含量(P＜0.05)也明显降低;与模型组比较,L-Arg可显著增加糖尿病大鼠肝、心肌、膈肌线粒体GSH-Px活性(P＜0.05,P＜0.05,P＜0.001)及肝、膈肌线粒体Mn-SOD活性(均P＜0.001),并使膈肌线粒体MDA含量显著降低(P＜0.01),而GSH含量明显升高(P＜0.001). 结论糖尿病大鼠肝、心肌、膈肌线粒体内自由基生成增多;L-Arg可通过提高肝、心肌、膈肌细胞线粒体中自由基清除酶的活性来加速自由基的清除,提高机体的抗氧化能力,从而保护机体功能免受氧化损伤.

The protective L-arginine on diabetes rats' mitochondria injury in liver and myocardium and diaphragm induced by free radicals

Objective To explore the protective effects of L-arginine ( L-Arg) on diabete rats'mitochondria injury in liver and myocardium and diaphragm induced by free radicals. Methods The diabetic model rats injected by alloxan were randomly divided into diabetes group, L-Arg treatment group and normal control group. The rats were killed 4 weeks later after using L-Arg to detect the activities of Mn SOD, GSH-Px and the levels of MDA in mitochondria of liver and myocardium and diaphragm and contents of GSH in mitochondria of diaphragm. Results The activities of GSH-Px decreased significantly (P<0.01, P<0.05, P<0.001 respectively) and the levels of MDA increased remarkably (P <0. 01, P <0. 05 , P <0. 01 respectively) in mitochondria of liver and myocardium and diaphragm in diabetic rats, and the activities of Mn-SOD in mitochondria of liver and diaphragm (allP<0.01) and the levels of GSH in mitochondria of diaphragm ( P < 0. 05 ) reduced obviously too compared with those of control group. The activities of GSH-Px increased remarkably in mitochondria of liver and myocardium and diaphragm ( P < 0. 05 , P < 0. 05 , P < 0.001 respectively) and the activities of Mn-SOD also increased obviously in mitochondria of liver and diaphragm ( all P < 0.001) , but the content of MDA in mitochondria of diaphragm obviously decreased ( P < 0. 01) and the levels of GSH increased (P <0. 001) in mitochondria of diaphragm in L-Arg treatment group compared with those of diabetic group. Conclusions The production of free radicals increase in mitochondria of liver and myocardium and diaphragm in diabetic rats. L-Arg could accelerate the free radical elimination through increasing the activities of SOD and GSH-Px in mitochondria of liver and myocardium and diaphragm to enhance the anti-oxidative function and protect from oxidative damage.