黄芪甲苷对缺血再灌注诱导的大鼠心肌损伤及细胞自噬的调节作用

Regulatory Effects of Astragaloside on Myocardial Injury and Cell Autophagy Induced by Ischemia-reperfusion in Rats

目的观察黄芪甲苷对缺血再灌注模型损伤大鼠心肌组织的保护作用及与心肌组织细胞自噬的关系。方法结扎大鼠左冠状动脉前降支建立心肌缺血再灌注损伤模型,采用细胞生物学及免疫组织化学法,观察心肌组织在缺血再灌注损伤模型及黄芪甲苷处理后的心肌组织损伤、细胞自噬的变化。结果缺血再灌注损伤使大鼠心肌组织中心肌灶性病变严重,兼有波浪改变及大片炎症细胞浸润,与假手术组相比损伤面积明显增多(P<0.05),而黄芪甲苷低、高剂量组均可使心肌灶性病变和炎症细胞浸润的面积明显减少(P<0.05)。Western blot结果显示,缺血再灌注损伤可激活心肌组织细胞中Beclin1的表达(P<0.05),而黄芪甲苷低、高剂量组均可降低缺血再灌注损伤诱导的心肌组织细胞Beclin1表达(P<0.05)。结论黄芪甲苷可在一定程度上减少缺血再灌注损伤的心肌面积,其机制可能是通过调节与自噬相关的Beclin1细胞信号转导通路而发挥作用。

Objective To explore the protection effects of astragaloside on injured myocardium induced by ischemia reperfusion and the relationship between myocardium cel autophagy and astragaloside.Methods The model of myocardial ischemia reperfusion was established by legating the left anterior descending coronary of rats.And,The changes of cardiomyocyte autophagy and injury in ischemia model after being treated with medicated serum were observed by molecular biology and immunocytochemical methods.Re-sults The ischemia reperfusion injury induced the severe myocardium local necrosis,wave shape change and blockbuster inflam-mation cel s infiltration.Compared with sham operation group,lesion area increased clearly(P<0.05).The area of myocardium local necrosis and inflammatory cel infiltration reduced obviously in low or high dose group of astragaloside(P<0.05).The result of west-ern blot test showed the expression of beclin 1 in cardiomyocytes was activated by ischemia reperfusion injury(P<0.05).The ex-pression of beclin 1 in cardiomyocytes induced by ischemia reperfusion injury was decreased in the low or high dose group of astra-galoside(P<0.05).Conclusion To some degree,astragaloside can reduce the area of injured myocardium induced by ischemia reperfusion.The mechanism may be by regulating the signal transduction pathway of beclin 1 cel related with autophagy.