耐力训练预防急性酒精性肝损伤机制:线粒体生物合成

Involvement of Endurance Training-Induced Liver Mitochondrial Biogenesis in Prevention of Alcohol-Induced Acute Hepatic Injury in Rat

目的:研究耐力训练对肝脏线粒体生物合成能力的影响及与急性酒精性肝损伤的关系。方法:以SD大鼠建立急性酒精性肝损伤模型,以12周无负重游泳为运动手段,测定其肝脏及血液相关指标的变化。结果:未训练大鼠急性酒精摄入导致肝脏与血液ALT、AST、MDA、线粒体ROS生成及态4呼吸升高,GSH含量、态3呼吸和RCR降低,线粒体生物合成蛋白PGC-1α、NRF1、TFAM和COXIVmRNA表达升高;耐力训练后再给予急性酒精摄入,使大鼠肝脏与血液ALT、AST、MDA、线粒体ROS生成及态4呼吸显著低于直接急性酒精摄入大鼠,GSH含量、态3呼吸和RCR显著高于直接酒精摄入大鼠,线粒体生物合成蛋白PGC-1α、NRF1、TFAM和COXIVmRNA表达显著高于未训练急性酒精摄入大鼠。结论:耐力训练能提高肝脏线粒体生物合成能力,进而保护线粒体的功能,从而达到部分预防急性酒精性肝损伤的目的。

This paper is to study the influence if endurance training liver and mitochondrial and its relations with acute hepatic injury. With this it establishes acute hepatic injury model in rats. It shows that acute alcohol intake for untrained rats leads to the increase of liver, blood ALT, AST, MDA, ROS transformation and model 4, while the decrease of GSH intake, model 3 breath and RCR. After endurance training an acute alcohol induction is siginificantly higher than direct and acute alcohol induction in LAT, AST, MDA, model 3, RCR and model 4. Therefore, endurance training can improve the composition ability of liver mitochondrial biogenesis so as to partially prevent the alcohol-induced acute hepatic injury.