参松养心胶囊对心肌梗死大鼠心肌细胞的保护作用

Protective Effect of Shensongyangxin Capsule on Cardiomyocytes in Rats with Myocardial Infarction and Its Possible Mechanism

目的探究参松养心胶囊对心肌梗死模型大鼠心肌细胞的保护作用及其可能的机制研究。方法采用冠状动脉前降支结扎术建立心肌梗死模型。将60只SD大鼠随机分为梗死组与非梗死组,非梗死组采取开胸后冠状动脉穿线,但不做结扎。模型制作成功后,将两组随机平分为对照组10只,美托洛尔组10只,参松养心胶囊组10只,术后分别以普食、普食+美托洛尔、普食+参松养心胶囊原粉喂食。8周后处理大鼠,取心肌梗死周围组织,检测各组大鼠心肌缝隙连接蛋白(Cx43)和信使RNA(mRNA)的表达量。结果在非梗死各组中Cx43蛋白表达强烈,且均匀的分布在细胞与细胞之间的连接处;与非梗死组比较,梗死组的对照组Cx43表达明显减弱,甚至全部消失,而参松养心胶囊组及美托洛尔组梗死区的Cx43表达减弱和分布的紊乱弥散程度均较小;非梗死各组的蛋白和mRNA表达水平差异无统计学意义(P>0.05);在梗死组中,对照组Cx43蛋白和mRNA表达明显低于参松养心胶囊组及美托洛尔组(P<0.05),但参松养心胶囊组与美托洛尔组之间差异无统计学意义(P>0.05)。结论参松养心胶囊能够显著改善大鼠心肌梗死后Cx43的表达,可能与其报道中能改善心肌梗死后心律失常和心功能不全有关。

Objective To investigate the protective effect of Shensongyangxin capsule on cardiomyocytes in rats with myocardial in-farction and its possible mechanism. Methods The model of myocardial infarction was established by anterior descending coronary artery ligation. Sixty SD rats were randomly divided into infarct group and non-infarct group. The non-infarct group was treated with thoracotomy coronary artery but not ligated. After the model was successfully made, the two groups were randomly divided into control group （ n= 10 ）, metoprolol group （ n= 10 ） and Shensongyangxin capsule group （ n= 10 ）. fed with normal diet, normal diet 〉 mato- prdol, or normal diet 〉 shensong yangxin after operation. The expression of Cx43 protein and mRNA in the myocardium aroundinfar- tionregion of rats were measured after 8 weeks of treatment. Results The expression of Cx43 protein in the non-infarct group was high-er and distributed evenly between the cells and the cells. Compared with the non-infarct groupfthe expression of Cx43 in the infarct group was significantly decreased and even disappeared（ P 〉 0.05 ）. In the infarct group,the expression of Cx43 in the infarcted area of the Shenshenyangxin capsule group and the metoprolol group were less than that in the non-infarct group （ P 〈 0.05 ）,but there was no significant difference between the Shenshenyangxin capsule group and the metoprolol group （ P 〉 0.05 ）. The expression of Cx43 protein and mRNA in the control group was significantly lower than that in the Shenshenyangxin capsule group and metoprolol group （ P 〈0.05 ）. Conclusions Shensongyangxin Capsule can improve the arrhythmia and cardiac dysfunction after myocardial in-farction. The possible mechanism is related to the regulation of Cx43 expression in cardiomyocytes .