硝酸异山梨酯通过20-HETE调控内皮祖细胞促进心肌梗死大鼠血管新生  

Isosorbidedinitrate Promotes Angiogenesis after Myocardial Infarction Through 20-HETE Regulated-endothelial progenitor cells Mobilization In Rats

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》2015年第5期359-360,372,共3页Lingnan Journal of Emergency Medicine

基　　金：国家自然科学基金(81370837;81170647);中国医师协会探索心血管研究基金(DFCMDA201238)

摘　　要：目的:通过建立大鼠心肌梗死模型,以流式细胞和免疫组化等方法探讨硝酸异山梨酯通过20-HETE调控内皮祖细胞促进血管新生的能力。方法:通过结扎冠脉前降支构建大鼠心肌梗死模型并给予ISDN及20-HETE特异性抑制剂(HET0016)干预8周,观察梗死面积、梗死交界区微血管密度及循环血中EPCs的数量。结果:ISDN有助于缩小心梗面积,增加梗死交界区微血管密度及循环血中的EPCs数量,20-HETE特异性抑制剂可部分阻断ISDN的效应。结论:ISDN可通过20-HETE调控EPCs促进血管新生。Objective： To explore whether isosorbidedinitrate （ISDN） 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. ISDN and a specific inhibitor of 20-HETE biosynthesis （HET0016） were administrated for eight weeks after MI surgery. Infarction area,microvascular density and the number of EPCs in the circulating blood were detected. Results：ISDN reduced the area of myocardial infarction, increased microvascular density in the border area of MI and the number of circulating EPCs in MI rats. However, 20-HETE biosynthesis inhibitor can partly block effect of ISDN. Conclusion： ISDN can promote angiogenesis by 20-HETE regulated-EPC smobilization.

关 键 词：硝酸异山梨酯 内皮祖细胞 血管新生 

分 类 号：R542.22[医药卫生—心血管疾病]