冠心舒通胶囊对大鼠心肌缺血再灌注损伤细胞凋亡影响的实验研究

Experimental Study of Guanxinshutong Capsule on Myocardial Apoptosis by Ischemia-Reperfusion in Rats

目的:探讨冠心舒通胶囊对大鼠心肌缺血再灌注(I/R)损伤细胞凋亡的影响。方法:30只雄性SD大鼠随机分为假手术组(10只)、模型组(10只)、药物组(10只)。模型组和药物组大鼠通过穿线结扎左冠状动脉前降支与松开的方法制备心肌缺血再灌注损伤模型(心肌缺血30min,再灌注3h)。假手术组只穿线不结扎。药物组大鼠在模型建立前5天开始每天给予冠心舒通胶囊,每次按1.5g/kg取药,溶于生理盐水,6mL/kg灌胃,每天两次,假手术组和模型组只给予同等剂量的生理盐水灌胃。各组心肌缺血30min,再灌注3h取材,采用缺口末端标记法(TUNEL)检测心肌细胞凋亡指数(AI);免疫印迹法(Western blot)检测Bcl-2、Bax基因蛋白的表达。结果:与假手术组比较,模型组Bax表达增强,Bcl-2表达减弱(P<0.01);与模型组比较,冠心舒通胶囊组,AI、Bax表达下降(P<0.01),Bcl-2表达上调(P<0.05)。结论:冠心舒通胶囊通过抑制心肌细胞凋亡,下调Bax基因蛋白表达,上调Bcl-2基因蛋白表达,起到心肌缺血再灌注损伤的保护作用。

Objective ：To study the effects of Guanxinshutong capsule （GXST） on myocardial apoptosis by ischemia -reperfu- sion（I/R） in rats. Methods：Thirty healthy male Sprague Dawley rats were randomly divided into three groups： Sham - operated group （10）, Model group （10）, and Drug group （10）. Myocardial ischemia reperfusion injury model was induced by the ligation of left descending anterior coronary artery （LAD）for 30 min, followed by 180 min of reperfusion in Model and Drug groups. From five days before surgery, GXST （ 1.5g/kg, two times per day,for Drug group） or saline （ for Model and Sham - operated groups） was administered via direct gastric gavage. Apoptosis index（AI） of myocardium was detectd by TUNEL method and the expression of apoptosis - related proteins Bcl-2, Bax were detected with the methods of Western Blot. Results ： Compared with sham - operated group, protein expression of Bcl-2 gene in Model group were reduced, and protein expression of Bax gene was increased （ all P 〈 0. 01 ）. compared with Model group, protein expression of Bcl-2 gene in Drug group were significantly increased（ P 〈 0. 05 ） ;apop- tosis index （AI） and protein expression of Bax gene was decreased （all P 〈 0. 01 ） ;Conchasion： GXST capsule can protect myocardium damage induced by I/R injury. The mechanism of cardioprotection may be associated with inhibiting apoptosis of myocar- dium, upregulating protein expression of Bel-2 gene and down regulating protein expression of Bax gene.