代谢综合征大鼠肝细胞线粒体损伤和mt DNA编码蛋白的表达变化

目的 通过观察代谢综合征(MS)大鼠肝细胞线粒体的损伤性改变及部分线粒体基因(mt DNA)编码蛋白的表达情况,探讨线粒体结构和功能改变的可能机制及其在MS发病中的作用.方法 采用经典的饮食诱导法建立喂养型MS大鼠模型.动态监测大鼠收缩压(SBP)、空腹血糖(FBG)、甘油三酯(TG)和高密度脂蛋白胆固醇(HDL-C)...

The hepatocyte mitochondrial injury and the expression of mt DNA encoding proteins in metabolic syndrome rats

Objective To observe the mitochondrial injury and the expression of mt DNA encoding proteins in hepatocyte of Wistar rat to explore the underlying mechanism and its effects on metabolic syndrome （MS）. Methods The Wistar rats were fed on the high-fat, high-sugar and high-salt diet, and the systolic blood pressure （SBP）, fasting blood glucose （FBG）, triglycercide （TG） and high-density lipoprotein cholesterol （HDL-C） were dynamically monitored to identify the MS rats. Then the hepatocytes of the MS rats were isolated for the following experiments： observing the morphological changes of mitochondrion under dectron microscope and analyzing the mitochondrial injury semi-quantitatively, detecting the expression of mt DNA encoding protein NADH dehydrogenase 1 （ND1）, cytochrome c oxidase 2 （COX2） and the subunit 1 of mitochondrial complex HI （Complex HI 1） by Western blotting. Results Mitochondrion swelling, vacuolar degeneration and the less crista or disappearance were observed in MS rat hepatocytes. The mitochondrial damage rate of MS and normal rat hepatocytes were 3.11 ＋ 0.31 and 0.30± 0.03 respectively （ P〈 0.01）. The expression levels of ND1 and COX2 in MS rats decreased significantly （P 〈0.05）, but the expression level of Complex Ⅲ 1 in MS rats increased significantly compared to the control （P〈0.05）. Conclusions The abnormally expressed mt DNA encoding proteins including ND1, COX2 and complex Ⅲ 1 might be related to the disorder of mitochondrial electron transfer and the increasing of electron leak. Thus, the excessive oxygen free radicals might induce the mitochondrial morphological changes and affect the metabolism through interfering the oxidative phosphorylation, which might be one of the possible mechanisms of MS.