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作 者:黄斐斐[1] 刘阳[2] 陈洁[3] 张坤[1] 张晋康[1] 王景峰[1] 黄辉[1]
机构地区:[1]中山大学孙逸仙纪念医院心内科,510120 [2]南华大学附属第二医院心内科 [3]中山大学孙逸仙纪念医院肿瘤放疗科
出 处:《岭南急诊医学杂志》2016年第1期4-6,24,共4页Lingnan Journal of Emergency Medicine
基 金:国家自然科学基金(81370837;81170647);中国中西医结合学会-和黄科研基金(2013002)
摘 要:目的:通过建立大鼠心肌梗死模型,探讨麝香保心丸(Shexiang Baoxin Pill,SBP)促进血管新生的效应和相关机制。方法:通过结扎冠脉前降支构建大鼠心肌梗死模型并给予SBP及20-HETE特异性合成抑制剂(HET0016)干预8周,观察心梗后心脏结构和功能、梗死交界区VEGF的变化及循环血中内皮祖细胞(endothelial progenitor cells,EPCs)的数量、20-HETE的变化。结果 :SBP可上调心梗后大鼠循环血中的20-HETE(0.35±0.02vs.0.56±0.04 ng/ml,P<0.05),有助于提高心梗后心脏射血分数[(46.3±4.20%vs.(62.30±3.40)%,P<0.05],增加梗死交界区VEGF(3.50±0.50 vs.9.80+1.00,P<0.05)及循环血中的EPCs的数量(0.16±0.06 vs.0.38±0.09,P<0.05),20-HETE特异性抑制剂可阻断SBP的效应。结论 :SBP可通过20-HETE调控EPCs促进血管新生。Objective:The present study was to explore whether Shexiang Baoxin Pill(SBP) could promote angiogenesis through 20-HETE mediated-endothelial progenitor cells(EPCs) mobilization in a rat model of myocardial infarct.Methods: Experimental myocardial infarction(MI) model was established in rats via occlusion of the left anterior descending coronary artery. SBP and a specific inhibitor of 20-HETE biosynthesis(HET0016) were administrated for eight weeks after MI surgery. Cardiac function was evaluated by echocardiography. The changes of VEGF in the border area of MI were measured. 20-HETE and EPCs in the circulating blood were detected. Results :SBP improved the heart ejection fraction [(46.3 ±4.20)% vs.(62.30 ±3.40)%, P〈0.05 ] after MI, increased VEGF(3.50 ±0.50 vs.9.80 +1.00, P〈0.05) and EPCs(0.16 ±0.06 vs. 0.38 ±0.09, P〈0.05) in the border area of MI 20-HETE biosynthesis inhibitor can block effect of SBP. Conclusion : SBP can promote angiogenesis by 20-HETE regulatedEPC smobilization.
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