活性氧的内源性心肌保护作用及其机制

Cardioprotection： reactive oxygen speciesin preconditioning and postconditioning

既往认为在心肌缺血/再灌注过程中活性氧是一种有害的细胞损伤因子,但最近研究发现也是可产生细胞保护作用的信号分子.活性氧（reactive oxygen species,ROS）在缺血,再灌注及其内源性心肌保护作用中具有双重作用,内源性心肌保护过程中活性氧主要来自线粒体呼吸链,主要通过mKATP-ROS通路产生;活性氧通过改变细胞氧化还原状态和调节线粒体膜通透性转换孔道开放状态,传递线粒体和细胞之间的信息联系.因此.活性氧不单是缺血/再灌注氧化应激的损伤因子,也是产生内源性心肌保护作用的重要信号分子.

In recent years the main idea has been that reactive oxygen species （ROS） play an essential,though double-edged, role in cardioprotection： they may participate in reperfusion injury or may play a role as signaling elements during myocardial adaptation to ischemia. It has been demonstrated that pre-or postconditioning triggering is redox-sensitive, via a mitochondrial KATP-ROS-dependent mechanism.In these cardioprotective phenomenon a redox signal and inhibition of mPTP are required during myocardial reperfusion following the index ischemic period. Therefore, the role of ROS in reperfusion may be reconsidered as they are not only deleterious.