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目的观察葛根素抑制心肌缺血/再灌注大鼠线粒体通透性转换孔对心肌细胞凋亡和自噬的影响。方法将40只SPF级SD大鼠随机分成假手术组,MIRI模型组,环孢霉素阳性对照组,葛根素组,每组10只;阻断大鼠升主动脉造成心肌缺血30 min,再灌注120 min造成大鼠心肌缺血再灌注损伤(Myocardial Ischemia reperfusion injury,MIRI)模型,采用环孢霉素和葛根素在结扎后5 min注射给药,测定各组心肌梗死面积,观察药物干预心肌线粒体通透性转换孔(mitochondrial permeability transition pore,m PTP)后对细胞色素C的释放、心肌细胞凋亡及自噬标志物LC3 II、Beclin1的影响。结果与MIRI模型组比较,葛根素组可以减少心肌梗死面积,抑制线粒体m PTP开放,减少细胞色素C水平和细胞凋亡指数,还可以降低自噬标志物LC3 II、Beclin1的表达(P<0.05),药理效果基本与环孢霉素阳性对照药类似。结论葛根素可以减少大鼠心肌缺血/再灌注梗死面积,其机制可能与抑制m PTP的开放,减少再灌注期心肌细胞大量凋亡和自噬有关。
Objective To investigate the effect of puerarin on cardiomyocyte apoptosis and autophagy in rats with myocardial ischemia / reperfusion injury. Methods Forty Sprague-Dawley (SD) SD rats were randomly divided into sham operation group, MIRI model group, cyclosporine positive control group and puerarin group, with 10 rats in each group. Blocking the ascending aorta caused myocardial ischemia for 30 min, Myocardial ischemia reperfusion injury (MIRI) model induced by 120 min reperfusion was induced by cyclosporine and puerarin at 5 min after ligation, and myocardial infarct size was determined in each group. Effects of mitochondrial permeability transition pore (m PTP) on cytochrome C release, cardiomyocyte apoptosis and autophagy markers LC3 II and Beclin1 were studied. Results Compared with MIRI model group, puerarin group could reduce myocardial infarct size, inhibit mitochondrial mPTP opening, decrease cytochrome C level and apoptosis index, and also reduce the expression of autophagy markers LC3 II and Beclin1 (P <0.05 ), The pharmacological effects of basic and cyclosporine positive control similar. Conclusion Puerarin can reduce myocardial ischemia / reperfusion infarction area in rats. The mechanism may be related to the inhibition of the opening of mPTP and the decrease of myocardial cell apoptosis and autophagy during reperfusion.