抑制COX-2表达对心肌缺血再灌注损伤过程中心肌细胞保护作用的研究

Protective effect of COX-2 inhibition on cardiomyocytes during myocardial ischemia-reperfusion injury

目的研究心肌缺血再灌注损伤过程中,环氧化酶-2(COX-2)表达水平与心肌细胞损伤之间的分子机制。方法通过缺氧/复氧(H/R)实验,模拟心肌缺血再灌注过程,在H9C2心肌细胞系中检测COX-2及其相关蛋白的表达水平,并通过COX-2特异性抑制剂NS398抑制其活性,观察细胞变化情况,并研究其作用机制。结果NFκB的激活诱导COX-2表达上调,COX-2促进H/R介导的促炎症因子转录,以及ROS活性增强。结论心肌细胞受到H/R刺激时,NFκB的激活诱导COX-2表达上调,抑制COX-2活性能够降低H/R诱导的促炎症因子转录以及ROS活性增强,从而发挥对心肌细胞的保护作用。

Objective To study the underlying molecular mechanism between cyclooxygenase-2(COX-2)expression and cardiac damage during myocardial ischemia-reperfusion injury(MI/RI).Methods The hypoxia/reoxygenation(H/R)experiment was used to simulate the process of MI/RI,and the expression of COX-2 and its related proteins was detected in H9 C2 cardiomyocyte cell line.In addition,NS398,specific inhibitor of COX-2,was used to inhibit the COX-2 expression.Further changes in cells were detected,and the underlying molecular mechanism was explored.Results The up-regulation of COX-2 expression was induced by the activation of NFκB during H/R,which promotes the transcription of inflammatory factors and the activity of ROS.Conclusion The higher COX-2 expression was induced by the activation of NFκB during H/R.Inhibition of COX-2 reduces the transcription of inflammatory factors and the activity of ROS,and finally attenuates myocardial cell injury.