【摘要】 目的观察从肝治心组方(CGZXP)对急性心肌梗死大鼠心肌微血管密度和血管内皮细胞生长因子(VEGF)的影响。方法复制大鼠急性心肌梗死模型,分别设CGZXP组、生理盐水(NS)组,7d及14d后分别取材(梗死与非梗死区交界处、梗死中心区心肌组织),用碱性磷酸酶(ALP)组织化学和免疫组织化学法,LEICAQ550CW图像分析系统分析缺血心肌微血管密度、VEGF蛋白表达情况,同时比较用药前后心肌梗死面积的变化。结果CGZXP组7d、14d单位面积微血管密度、VEGF蛋白表达均较NS组明显增加(P<0.01),并能相应减少心肌梗死的面积,对梗死中心区心肌的血管生成作用弱于梗死与非梗死交界部位。结论本研究初步证实CGZXP能促进实验性心肌梗死大鼠缺血心肌微血管生成,缩小心肌梗死面积;CGZXP对VEGF表达的上调可能是其血管生成的作用机制之一。更多还原

【Abstract】 To study the effect of Congganzhixin Prescription(从肝治心组方,CGZXP) on myocardial microvessel density(MVD) and vascular endothelial growth factor(VEGF) of rats with acute myocardial infarction(AMI). Methods:All of AMI model rats were divided into CGZXP group and normal saline(NS) group randomly. 1 and 2 weeks after therapeutics,dispart the border and center of infracted myocardium,MVD and Average O.D. of VEGF were assayed by Alkaline phosphatase(ALP) histochemical methods and Immunohistochemical stain using digital analysis system,the infarcted area was compared at the same time. Results:Both time MVD and the expression of VEGF of CGZXP were increased significantly than those of the controlled group,and myocardial infarct area was significantly decreased in CGZXP group. Conclusion:CGZXP could promote angiogenesis and decrease myocardial infarct area,upregulation of VEGF protein might be a potential mechanism of CGZXP in protection of infracted myocardium.更多还原