通心络对心肌梗死模型大鼠心肌损伤保护作用及机制的研究

Protective effect and mechanism of Tongxinluo on myocardial injury in myocardial infarction model rats

目的探索通心络对心肌梗死模型大鼠心肌损伤的保护作用及机制。方法采用结扎前降支方法制作30只心肌梗死大鼠模型,随机分为模型组、通心络组、培哚普利组,每组10只;假手术组9只仅穿线不结扎。药物组大鼠分别以通心络、培哚普利灌胃,模型组和假手术组给予等量羧甲基纤维素钠溶液灌胃。2周后测量TUNEL凋亡指数,以及血清超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(malondialdehyde,MDA)、一氧化氮(nitrogen monoxide,NO)、内皮素-1(endothelin-1,ET-1)水平。结果药物组大鼠的一般情况均有所改善。通心络组、培哚普利组的凋亡指数和MDA、ET-1水平较模型组均明显降低,SOD、NO水平较模型组均明显升高(P<0.05)。结论通心络可抑制心肌细胞凋亡,并通过升高SOD、NO水平,降低MDA、ET-1水平,改善氧化应激状态和内皮功能,保护心肌组织。

Objective To study the protective effect and mechanism of Tongxinluo on myocardial injury in myocardial infarction model rats. Methods The rat model of acute myocardial infarction was established by ligaturing the left anterior descending coronary artery. 30 model rats were randomly divided into the model group,Tongxinluo group,Perindopril group,10 rats in each group. And 9 rats in sham group were punctured only without ligation. The rats in each medication group were intragastric administration respectively by Tongxinluo suspension and Perindopril suspension with corresponding dosage. And the model group and the sham group were intragastric administration by sodium carboxymethyl cellulose solution with corresponding dosage. All the rats were given continuously for 2 weeks. The apoptotic index and the level of SOD,MDA,NO and ET-1 were measured by corresponding methods. Results The general condition of rats in medication groups was better than model group. The level of SOD and NO in Tongxinluo group and Perindopril group was increased more significantly than that of the model group（ P〈0. 01）. The level of MDA and ET-1 in Tongxinluo group and Perindopril group was decreased more significantly than model group（ P〈0. 05）. Conclusions Tongxinluo can inhibit myocardial apoptosis,and protect the cardiacmuscle tissue by increasing the level of SOD and NO,decreasing the level of MDA and ET-1,and it also can improve the oxidative stress and perform protective effect on myocardial tissue endothelial function.