中文摘要：

目的观察远志皂苷元（senegenin,SEN）对小鼠心肌缺血再灌注损伤的保护作用,并深入探讨远志皂苷元作用的分子机制。方法实验分组：对照组（穿线不结扎,空置225min）、模型组（冠状动脉左前降支结扎45min,再灌注180min）和SEN处理组（冠状动脉左前降支结扎45min,再灌注前10min给予静脉注射30mg/kg远志皂苷元,再灌注180min）。采用伊文氏蓝-TTC双染法测定心肌梗死面积;荧光分析法检测Caspase-12和Caspase-3的活性以评价小鼠心肌细胞的凋亡情况;采用免疫印迹法检测心肌梗死区内质网应激标志蛋白GRP78和CHOP的表达水平。结果与对照组相比,模型组小鼠心肌梗死区的面积显著增大,Caspase-12和Caspase-3活性分别增高了4.71倍和3.37倍,内质网应激相关的标志蛋白GRP78和CHOP表达水平亦显著增高。与模型组相比,SEN处理组小鼠心肌缺血再灌注损伤导致的心肌梗死面积、Caspase-12和Caspase-3的活性程度均显著降低,GRP78和CHOP的表达水平亦显著降低,差异具有统计学意义（P〈0.05或P〈0.01）。结论远志皂苷元对小鼠心肌缺血再灌注损伤具有明显的保护作用,其可能的机制与改善心肌内质网应激介导的细胞凋亡有关。

英文摘要：

Objective To investigate the protective role of senegenin（SEN）in the mouse ischemia-reperfusion injury and its mechanism.Methods Mice were divided at random into control group（the ligature was placed but not ligated for 225min）,ischemia-reperfusion model group（the anterior descending coronary artery remained ligated for 45 min and then reperfused for 180min）and SEN treatment group（30mg/kg SEN was used 10 min before reperfusion）.The myocardial infarct size was measured by using Evans blue-TTC staining.Fluorescence assay was employed to detect the activity of Caspase-12 and Caspase-3to assess the myocardial apoptosis.Western blot was used to detect the expression of two endoplasmic reticulum stress（ERS）markers,GRP78 and CHOP,in infarcted myocardia.Results Compared with the control group,the myocardial infarct size was significantly increased,the activities of Caspase-12 and Caspase-3were increased by 4.71 fold and 3.37 fold,respectively,and the expression levels of ERS markers GRP78 and CHOP were conspicuously elevated in the ischemia-reperfusion model group.Pretreatment with SEN（30mg/kg）could significantly reduce the myocardial infarct size,the activities of Caspase-12 and Caspase-3and the expression levels of GRP78 and CHOP when compared with those in the ischemia-reperfusion model group and there was significant difference between the two groups（P〈0.05 or P〈0.01）.Conclusion SEN can protect against the myocardial ischemia-reperfusion injury by ameliorating ERS-mediated myocardial apoptosis in mice.