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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 role and mechanism of cyclooxygenase (COX) 1,2 in the process of ischemic myocardial angiogenesis and endothelial progenitor cell mobilization. Methods The experimental rats were randomly divided into three groups: ropinoxifexim, a selective COX2 inhibitor for myocardial ischemia, valeryl salicylate (VS), a selective COX1 inhibitor, and myocardial ischemia. Myocardial ischemia group was given plasma VEGF for 1 week after operation. Peripheral blood mononuclear cells were counted for culture. Endothelial progenitor cells and ischemic myocardium were counted for hypoxia inducible factor-1α mRNA. After 28 days, ischemic area Myocardial immunohistochemistry to measure capillary density. Results Compared with myocardial ischemia plus VSMC group, the levels of VEGF, circulating EPCs, myocardial capillary density and hypoxia inducible factor-1α mRNA (P <0.05). There was no significant difference between the other two groups. Conclusions COX2 plays an important role in the mobilization of endothelial progenitor cells and myocardial angiogenesis in ischemic myocardium. The possible mechanism is that COX1 has no effect on the expression of hypoxia inducible factor-1α and VEGF.