复方黄芪养心合剂对大鼠缺血再灌注心肌缝隙连接蛋白43的影响

Effects of reperfusion arrhythmias and myocardial connexin 43 by Compound Astragalus Mixture Nourishing Heart in a rat model of acute myocardial ischemic reperfusion injury

目的:观察复方黄芪养心合剂对SD大鼠缺血再灌注心肌细胞缝隙连接蛋白43(Cx43)分布的改变和表达的影响。方法:应用复方黄芪养心合剂按每天14g/kg剂量、琥珀酸美托洛尔缓释片按每天(MSSRT)9.5mg/kg剂量灌胃2周后,对SD大鼠行冠状动脉左前降支结扎30min后再灌注60min造成心肌缺血再灌注(I/R)损伤模型,记录Ⅱ导联心电图,采用免疫组织化学法(IHC)观察心肌细胞Cx43分布的改变;运用Image Pro Plus 6.0图像分析软件对Cx43的表达进行半定量分析。结果:Cx43平均光密度(AOD)I/R组心肌内膜下缺血区Cx43的AOD显著低于假手术组(P<0.01),且MSSRT组、复方组较1/R组升高(P<0.05)。结论:对冠状动脉左前降支结扎术后再灌注SD大鼠,复方黄芪养心合剂对心肌细胞Cx43分布的改变有改善作用,有促进心肌内膜下缺血区域Cx43表达的作用,其作用与MSSRT相近。

Objective： To evaluate the effects of Compound Astragalus Mixture Nourishing Heart （CAMNH） antiarrhythmia and myocardial connexin 43 （Cx43） in a rat model of acute myocardial isehemic reperfusion injury. Methods： Myocardial infarction （MI） was induced by ligating left anterior descending coronary artery （LAD） for 30 minutes, followed by reperfusion of 60 minutes in rats. Rats were treated with CAMNH （14g·kg^-1·d^-1） or metoprolol succinate sustained-release tablets （MSSRT, 9.5mg·kg^-1·d^-1） for 14 days before MI. The distribution of myocardial Cx43 was observed by Immunohistochemistry （IHC）, and the expression of myocardial Cx43, which were represented by average optical density （AOD）, was measured by Image Pro Plus 6.0. Results： The expression of myocardial Cx43 in infarction region was significantly reduced, disordered and even all disappearing, the expression of myocardial Cx43 from infarction region into ischemic region and normal region had a gradual recovery of transitional variability. Ischemia/reperfusion（I/R） group vs sham-operated （SO）group, AOD of myocardial Cx43 in subendocardial region was significantly reduced （P〈0.01）. CAMNH group and MSSRT group vs I/R group, the change of the distribution of myocardial Cx43 was modified, and AOD of myocardial Cx43 in ischemic region was increased （P〈0.05）, but AOD of myocardial Cx43 in normal region was not altered. Conclusion： CAMNH, in a rat model of ischemic reperfusion injury, modifies the distribution of myocardial Cx43, increases the expression of myocardial Cx43 in ischemic region, and the effects is near to MSSRT.