【摘要】 目的观察蛇床子素后处理对大鼠心肌急性缺血/再灌注损伤心肌细胞凋亡的影响,并对其可能的作用机制进行探讨。方法结扎大鼠左冠状动脉前降支30 min后,松开结扎线再灌注120 min制备急性心肌缺血/再灌注损伤模型;将30只Wistar大鼠随机分为以下3组:对照(Sham)组、缺血/再灌注(I/R)组、I/R+蛇床子素后处理(Ost)组。采用TUNEL法原位标记缺血区凋亡心肌细胞并计算凋亡指数,采用Western blot法检测心肌组织中Caspase-3、Bcl-2及Bax三种蛋白的表达。结果与Sham组相比,I/R组心肌细胞凋亡指数、心肌组织Caspase-3蛋白、Bcl-2蛋白和Bax蛋白含量明显增高(均P<0.05);与I/R组相比,Ost组心肌细胞凋亡指数(P<0.05)、心肌组织Caspase-3蛋白(P<0.01)及Bax蛋白表达水平均降低(P<0.05),而Bcl-2蛋白表达水平明显增高(P<0.05)。结论蛇床子素后处理能抑制急性心肌缺血/再灌注损伤所致的大鼠心肌细胞凋亡,同时上调心肌组织中Bcl-2蛋白的表达及下调心肌组织中Bax蛋白的表达,提示上调Bcl-2蛋白及下调Bax蛋白、进而上调Bcl-2/Bax比值可能是其发挥抗心肌细胞凋亡作用的机制。更多还原

【Abstract】 Objective To investigate the effects of Osthole postconditioning on cardiomyocyte apoptosis induced by ischemia/reperfusion in rats,and to study the possible mechanism.Methods The acute myocardial ischemia/reperfusion rat models were established by ligating anterior decending branch of left coronary artery for 30 min and then reperfused 120 min.30 Wistar rats were randomly divided into Control(Sham)group,Ischemia/reperfusion(I/R)group and I/R+Osthole postconditioning(Ost)group.Cardiomyocyte apoptosis was determined by TUNEL staining and Caspase-3 expression.The expressions of Caspase-3,Bcl-2 and Bax protein in the myocardium were detected by Western blot technique.Results Compared with the Sham group,the apoptotic index(AI),the expression of Caspase-3,Bcl-2 and Bax protein in myocardial tissues were significantly increased in I/R group(P<0.05).Compared with I/R group,the apoptotic index(AI)(P<0.05),the expression of Caspase-3(P<0.01)and Bax protein in myocardial tissues(P<0.05)was decreased significantly,while Bcl-2 protein(P<0.05)was increased significantly in Ost group.Conclusions The present study find that Osthole postconditioning decrease cardiomyocyte apoptosis induced by acute ischemia/reperfusion injury in rats,up-regulate the expression of Bcl-2 protein and down-regulate the expression of Bax protein,which suggest the cardioprotection effects of osthole postconditioning might be associated with up-regulating the expression of Bcl-2 protein,down-regulating the expression of Bax protein,and then raising the ratio of Bcl-2/Bax.更多还原