游泳训练改善Ⅱ型糖尿病大鼠心肌线粒体重塑  

The Effect of Swimming Training on Myocardial Mitochondrial Remodeling in Rats with Type Ⅱ Diabetes

作　　者：缪本海[1] 

机构地区：[1]广东水利电力职业技术学院体育教学部,广东广州510000

出　　处：《首都体育学院学报》2014年第1期85-90,共6页Journal of Capital University of Physical Education and Sports

基　　金：河南省科技攻关项目(112102310694)

摘　　要：耐力训练可纠正多种病理因素导致的线粒体功能异常,然而,其对II型糖尿病(DI)心肌线粒体的影响仍不清楚。通过建立DI模型并采用游泳训练作为干预手段,检测耐力训练对DI心肌线粒体的保护作用并分析其内在机制。将80只Wistar大鼠在完成Ⅱ型糖尿病造模后,随机分成3组:正常对照组(CON);糖尿病组(DI);糖尿病+游泳训练组(DI+SW)。训练方案为:60min/d,每周5d,共计8周。检测线粒体功能,动力学蛋白,数量及质量控制体系(合成和自噬)的变化。结果发现:DI后,线粒体复合物Complex I,III活性显著性降低;线粒体动力蛋白mfn1/2表达降低,DRP1显著性升高;线粒体数目(蛋白MnSOD和VDAC)显著性降低;线粒体合成(蛋白PGC-1α,Tfam)明显降低;自噬信号通路ERK1/2-JNK-p53被激活,自噬水平(蛋白Atg7,Bclin-1,LC3)显著性升高。相对的,SW可有效提高线粒体功能(Complex活性)。该效应与动力学蛋白改善(增加mfn1/2及降低DRP1表达),线粒体数量增加(上调MnSOD和VDAC表达)及质量调控体系的再平衡(增加合成蛋白PGC-1α,Tfam;失活ERK1/2-JNK-p53及降低自噬蛋白Atg7,Bclin-1及LC3表达)相关。得出结论:SW可有效改善DI造成的线粒体功能紊乱。其中,抑制动力学蛋白异常改变,增加线粒体数量及再平衡线粒体质量调控体系可能发挥重要作用。提示,SW可作为DI预防和治疗的有效手段。Objective： Endurance training has been proven to normalize mitochondrial dysfunctions caused by various pathological factors. However, its effects of on mitochondria under type 2 diabetes mellitus condition were still unclear. The present thesis sets to determine swimming training （SW）mediated pro tections for myocardial mitochondria in DI animals, and to explore the underling mechanisms. Method：Af ter DI model completion, 80 Wistar rats were randomly divided into three groups： normal control group （CON） ; type 2 diabetes mellitus group （DI） ; diabetes mellitus ＋ swimming training group （DI＋ SW）. Training protocol： 60 rain/d;5 d/week;Total of 8 w. Results：after DI,mitochondrial complex I, III activi ties were significantly decreased;network dynamic protein level of mfnl/2 were reduced; whereas, DRP1 was downregualted; mitochondrial biogenesis （PGC1 a, Tfam） depressed, but autophagy signaling ERK1/ 2 JNKp53 was activated, and autophagy level was increased, as supported by increased protein expres sions of Atg7, Bclin1, LC3. By comparison, SW effectively improves mitochondrial function （Complex ac tivities）, which was found to relate to improved mitochondrial dynamic proteins, increased mitochondrial volumes and rebalanced quality regulatory system. Conclusion： SW could improve DIcaused mitochondri al dysfunction. Of which, inhibitions of pathologically remodeled network proteins, maintenance of content and r^balance of quality regulating system may perform key roles. SW is expected to be an effective mo dality for DI prevention and treatment.

关 键 词：动力学蛋白 增殖 自吞噬 氧化应激信号通路 线粒体重塑 糖尿病 

分 类 号：G804.7[文化科学—运动人体科学]