摘要
目的探讨人参皂苷Rg1对心肌梗死大鼠冠状动脉新生血管形成的影响及其作用机制。方法结扎Wistar大鼠左冠状动脉制作急性心肌梗死(AMI)模型,应用人参皂苷Rg1动员自体骨髓干细胞,建模后第24小时、1周和4周时分别处死大鼠,取出心脏,HE染色检测梗死面积,免疫组化方法观察心肌梗死灶、边缘区和正常心肌组织CD34阳性细胞、VEGF及其受体的表达,以及Ⅷ因子表达。结果应用人参皂苷Rg1治疗后,治疗组大鼠心梗区可见CD34阳性细胞浸润;梗死面积明显减小;梗死灶及周围组织中微血管密度、VEGF及其受体(Flk-1)的表达量均明显高于AMI组及假手术对照组。结论在大鼠AMI模型中,应用人参皂苷Rg1治疗,可动员骨髓干细胞归巢于缺血心肌,有效促进微血管形成,通过上调VEGF和VEGF受体Flk-1的表达,促进血管再生,促进缺血心脏功能恢复。
Objective： To investigate the stimulate angiogenesis effect and mechanism of ginsenoside Rgl on coronary collateral development in the hearts of experimental myocardial infarction rats. Methods： Left anterior descending coronary arteries of wistar rats were ligated to produce acute myocardial infarction（AMI） model. Bone marrow stem cells were mobilized by ginsenoside Rgl. Hearts were harvested in the 24th hour, 1st and 4th week after AMI modeling for histopathological examination. Immunohistochemisty were used to detect infiltration of CD34 cells and the expression of VEGF and its receptors （Flk - 1 ）,Ⅷ factor in the part of ischemia. And infarct area were measured. Results：Infarct area in treatment group was obviously less than in AMI group. There were a great number of monocytes infiltrating with CD34 expression by immunohistochemisty in myocardial infracted zone in mobilized rats. Capillary density in treatment group was greater than those of AMI and sham - operated groups. Expression of VEGF and Flk - 1 was found in all group, but in treatment group the expression of VEGF and Flk - 1 enhanced obviously. Conclusion：In the AMI model of rat, bone marrow stem cells can be mobilized by ginsenoside Rgl. The capillary density can be increased by mobilizing bone marrow stem cells. And ginsenoside Rg1 can improve the acute ischemic cardiac function by upregulating the expressions of VEGF, Flk - 1 and enhancing angiogenesis.
出处
《中国中医急症》
2009年第3期403-405,共3页
Journal of Emergency in Traditional Chinese Medicine
基金
广东省汕头市重点科技计划项目(No.2007-76-39)
关键词
心肌梗死
人参皂苷RG1
骨髓干细胞
心肌血管再生
侧支循环
大鼠
Myocardial infarction
Ginsenoside Rgl
Bone marrow stem cells
Regeneration of myocardium and neovascularization
Coronary collateral development
Rats
