【摘要】 目的探讨益气活血汤对急性心肌梗死(AMI)模型大鼠缺血心肌Ras、ERKl(extracellularsignal regulated kinasel)、p-ERKl(phosphor-ERKl)和C-Raf-1蛋白表达的影响。方法将Wistar大鼠随机分为正常组、假手术组、模型组、倍他乐克组和益气活血汤大、小剂量组(下称大、小剂量组)。采用大鼠冠状动脉左前降支结扎构造急性心肌梗死(AMI)的心肌缺血模型。通过免疫组化法检测缺血心肌的Ras、ERKl、p-ERKl及C-Raf-1的蛋白表达。结果模型组Ras、ERKl、p-ERKl及CRaf-1的蛋白表达均高于空白组、假手术组,差异有统计学意义(P<0.05或P<0.01)。Ras、C-Raf-1蛋白表达:小剂量组与模型组比较差异无统计学意义(P>0.05);大剂量组及倍他乐克组与模型组比较均有增高(P<0.05或P<0.01)。ERK1、p-ERK1蛋白表达:大、小剂量及倍他乐克组与模型组比较均有增高,差异有统计学意义(P<0.05或P<0.01)。四个因子在大剂量组的表达均较小剂量组增多更明显(P<0.05)。结论益气活血汤可能是通过提高Ras通路相关蛋白表达来促进缺血后心肌的血管生成,抑制心肌缺血的损伤。更多还原

【Abstract】 Objective To study the effects of Yiqi Huoxue decoction(YQHXD) on the protein expressions of Ras,ERKl(extracellularsignal regulated kinasel), p-ERKl(phosphor-ERKl) and C-Raf-1 in acute myocardial ischemic(AMI) rats with ischemic myocardium. Methods Wistar rats were randomly divided into the normal group, sham-operated group, model group,betaloc group, low-dose YQHXD group, high-dose YQHXD group.Ischemic myocardium AMI rat models were formed by the ligation of the left anterior descending coronary artery. The protein expressions of Ras, ERKl, P-ERKl, and C-Raf-1 were examined by using immunohistochemistry. Results The protein expressions of Ras, ERKl, P-ERKl and C-Raf-1 in the model group increased significantly compared with the normal group and sham-operated group, the differences were statistically significant(P <0.05 or P <0.01). Expressions of Ras and C-Raf-1 protein between low dose YQHXD group and the model group had no statistical significance(P >0.05); while the high-dose and betaloc group was higher than that expressions in the model group(P<0.05 or P<0.01). The expressions of ERK1 and p-ERK1 in the high-dose, low-dose and the betaloc group were significantly higher than the model group(P<0.05 or P<0.01). The expressions of Ras, ERKl, P-ERKl and C-Raf-1 in the high-dose YQHXD group were significantly higher than the low-dose group(P <0.05). Conclusion YQHXD could probably up-regulate the protein expressions of important factors on Ras signal pathway to promote the angiogenesis of ischemic myocardium of ischemic myocardium and suppress the myocardial ischemia injury.更多还原