环氧化酶在大鼠缺血心肌血管生成及内皮祖细胞动员中的作用

The role of cyclooxygenase on angiogenesis and endothelial progenitor cell mobilization in rat ischemic myocardium

目的探讨环氧化酶(COX)1、2在缺血心肌血管生成和内皮祖细胞动员中的作用及机制。方法实验大鼠随机分为心肌缺血加选择性 COX2抑制剂罗非昔布组、心肌缺血加选择性 COX1抑制剂 valeryl salicylate(VS)组和单纯心肌缺血组。心肌缺血组于术后1周取血浆测血管内皮生长因子(VEGF),外周血分离单个核细胞培养计数内皮祖细胞和缺血心肌组织检测缺氧诱导因子-1αmRNA,28天后取缺血区心肌免疫组化法测毛细血管密度。结果心肌缺血加罗非昔布组与单纯心肌缺血组、心肌缺血加 VS 组比较,血浆 VEGF 水平、循环血内皮祖细胞计数、缺血心肌毛细血管密度和缺氧诱导因子-1α mRNA 表达均显著减少(P<0.05),其余指标两组差异无统计学意义。结论COX2在心肌缺血时内皮祖细胞动员和缺血心肌血管生成中起重要作用,其可能机制与增加缺氧诱导因子-1α和 VEGF 的表达有关,而 COX1没有作用。

Objective To investigate the effect of COX1 and COX2 on angiogenesis and endothelial progenitor cell mobilization in rats with experimental myocardial infarction （MI）. Methods The rats were randomly divided into 3 groups： MI group, MI plus rofecoxib group and MI plus valeryl salicylate group. At the 7th day after operation, circulating EPCs, plasma VEGF and HIF-1α mBNA of ischemic myocardium were measured. At the 28th day post operation, capillary densities were also measured in ischemic myocardium. Result Compared with the MI group and the MI plus valeryl salicylate group, circulating EPCs, plasma VEGF, HIF-1α mRNA and capillary densities of ischemic myocardium were all decreased in MI plus rofecoxib group. Conclusion The present study revealed that COX2 play an important role with angiogenesis and endothelial progenitor cell mobilization in rat with experimental MI by modulating expression of VEGF and HIF-1α .