芪桂益脉灵对急性心肌缺血再灌注损伤大鼠心肌细胞外信号调节激酶1/2的影响

Effect of Qigui Yimailing(芪桂益脉灵) on ERK1/2 in Rats with Acute Myocardial Ischemia-reperfusion Injury

目的:观察芪桂益脉灵对心肌缺血再灌注大鼠心肌组织细胞外信号调节激酶1/2(ERK1/2)的影响。方法:取SD大鼠50只,随机分为5组,正常对照组、假手术组、模型组、芪桂益脉灵高、低剂量组,分别给生理盐水、QGYML1.2 g/kg和0.6 g/kg),连续灌服7 d。结扎冠状动脉左前降支造成急性心肌梗死(AMI)模型。实验结束后免疫组化法检测心肌组织ERK1/2、P-ERK1/2的蛋白表达水平。结果:各组大鼠心肌ERK1/2蛋白表达水平比较无显著性差异(P>0.05);与正常组、假手术组比较,模型组心肌PERK1/2表达显著升高(P<0.05);芪桂益脉灵组P-ERK1/2表达显著高于空白组、假手术组和单纯缺血再灌注组,其中高剂量组升高更加明显(P<0.05)。结论:芪桂益脉灵能够升高ERK1/2磷酸化水平,减少心肌细胞的凋亡,对缺血再灌注损伤心肌具有保护作用。

Objective：To observe the effect of Qigui Yimailing（QGYML） on ERK1/2 in myocardial tissue of rats with ischemia reperfusion injury.Methods：50 SD male rats were randomly divided into 5 groups which each had 10 rats,normal group,sham operation group,model group （I/R）,QGYML low dose group （QL） and QGYML high dose group （QH）,with the physiological saline,QGYML1.2 g/kg or0.6 g/kg respectively for 7days.Acute myocardial infarction（AMI） models were caused by ligation of the left anterior descending branch of the coronary artery Immunohistochemical method was used to detect ERK1/2 and P-ERK1/2 protein expression levels in myocardial tissue.Results：ERK1/2 protein expression level was no significant difference in all the groups（P 〉0.05）;P-ERK1/2 expression in model group was enhanced significantly to compare with normal and sham groups （P 〈 0.05）,that in QGYML high and low dose groups was significantly higher than that in model group （P〈0.05）,the effect of high dose group was more significant than that of low dose group（P 〈0.05）.Conclusion：QGYML can raise ERK1/2 phosphorylation level,protect myocardial ischemia-reperfusion injury.