麝香保心丸对动脉粥样硬化斑块和缺血心肌中血管新生影响的实验研究

Effects of Shexiang Baoxin Pill on Angiogenesis in Atherosclerosis Plaque and Ischemic Myocardium

目的应用麝香保心丸干预动脉粥样硬化和心肌梗死动物双模型,同步观察麝香保心丸对动脉粥样硬化和缺血心肌中血管新生的影响。方法 20只雄性新西兰大白兔,制备动脉粥样硬化和心肌梗死双模型,随机分为两组。高脂组为高脂饮食对照组,保心丸组为高脂饮食加麝香保心丸药物干预组。测定心功能及主动脉弓斑块阳性面积。采用免疫组化染色测定梗死边缘区和主动脉血管壁CD34阳性反应强度,测定梗死边缘区新生血管密度。采用Westernblot检测血管内皮生长因子(VEGF)和血管内皮生长因子受体-2(VEGFR-2)的表达。结果保心丸组的心功能水平较高脂组改善,两组比较,差异有统计学意义(P<0.05)。保心丸组斑块阳性面积(%)为45.82±3.68,较高脂组(82.56±4.97)减少,差异有统计学意义(P<0.01)。在梗死边缘区,保心丸组的CD34阳性反应强度和新生血管密度高于高脂组,VEGF和VEGFR-2的表达亦强于高脂组(P<0.01);在主动脉血管壁,保心丸组的CD34阳性反应强度低于高脂组,VEGF和VEGFR-2的表达亦低于高脂组(P<0.01)。结论麝香保心丸能促进梗死边缘区血管新生,改善心功能;同时可抑制动脉粥样硬化斑块内血管新生。

Objective To investigate the effects of Shexiang Baoxin Pill （SBP） in intervening atherosclerosis and myocardial infarction （AS-MI） in experimental animals,and inspect its influences on angiogenesis.Methods Twenty male New-Zealand rabbits were made into AS-MI model,and randomly divided into 2 groups equally.Group A was fed with highfat diet for control;Group B was fed with high-fat diet but intervened with SBP.The cardiac function and the positive area of plaque were determined.The CD34 positive response intensity at infarcted marginal zone and aorta vessel wall,and the capillary density of myocardium were measured by immunohistochemical staining.In addition,the protein expressions of vascular endothelial growth factor （VEGF） and vascular endothelial growth factor receptor-2 （VEGFR-2） were detected by Western blot.Results Compared to Group A,the cardiac function was obviously improved （P0.05） and the plaque positive area （%） was significantly decreased in Group B （45.82±3.68 vs 82.56±4.97,P0.01）.The CD34 positive response intensity and the capillary density as well as VEGF and VEGFR-2 expressions in infarcted marginal zone in Group A were higher than those in Group B （P0.01）;but these parameters at aorta vessel walls were lower in Group A than in Group B （P0.01）.Conclusion SBP could advance the angiogenesis in the marginal zone of infarction,improve heart function,and embarrass angiogenesis in atherosclerotic plaque.