黄芪多糖抗心肌缺血再灌注损伤的线粒体机制研究

Astragalus Polysaccharides(APS) Protects Against Myocardial Ischemia-Reperfusion(I/R) Injury Through Mitochondrial Mechanisms

目的:通过观察黄芪多糖对缺血再灌注损伤大鼠心肌线粒体膜电位、膜通透性转换孔(mPTP)活性及钙离子浓度等指标的影响,以探索黄芪多糖产生心肌保护作用的线粒体机制。方法:健康成年SD雄性大鼠35只分为假手术组、缺血再灌注组、黄芪多糖预处理组、黄芪多糖后处理组、阳性药物腺苷对照组各7只,采用冠状动脉结扎的方法建立大鼠心肌缺血模型,测定心肌线粒体膜电位、线粒体膜通透性转换孔(mPTP)活性、线粒体钙离子浓度及ROS水平等指标。结果:与假手术组比较,缺血再灌注损伤组线粒体膜电位、mPTP的开放程度、线粒体钙离子浓度及ROS水平均显著升高,而经黄芪多糖处理后线粒体膜电位、mPTP的开放程度、线粒体钙离子浓度及ROS水平明显降低。结论:黄芪多糖可通过减轻钙超载,减少ROS产生,降低膜电位水平及抑制mPTP过度开放,从而减轻缺血再灌注损伤对线粒体膜结构的破坏,保护线粒体功能,进而保护心脏舒缩功能。

Objective ： To investigate the mitochondrial mechanisms of Astragalus Polysaccharides （APS） therapy by observing the effects on the expression of the mitochondrial membrane potential （MMP） , the active of mitochondrial permeability transition pore （mPTP） and the concentration of calciumion in rats with myocardial ischemia-reperfusion （ I/ R） injury. Methods： Thirty five （35） male Sprague-Dauley （SD） rats were randomly divided into the following 5 groups： sham operation group, I/R injury group, APS pre-treatment group, APS post-treatment group and adenosine control group. We measure the levels of MMP, the concentration of calciumion, the level of reactive oxygen species （ROS）, and the active of mPTP. Results： Compared with the sham operation group, the I/R injury group showed significantly increase with the lcvels of MMP, the concentration of calciumion, the level of reactive oxygen species （ROS） , and the active of minP. Compared with the I/R injury group, the APS pre-treatment group and the APS post- treatment group showed significantly decrease in all these indicators. Conclusion： APS play a protecting role on cardiac function through protecting the function of mitochondria, which by reducing the levels of ROS, the concentration of aealciumion, the level of MMP, and inhibiting the opening of mPTP.