核因子-κB介导心肌缺血再灌注损伤机制的研究进展

Mechanism of nuclear factor-κB mediated myocardial ischemia-reperfusion injury

炎症反应在心肌缺血再灌注损伤中起关键作用,贯穿于心肌细胞损伤的全过程。参与炎症反应的黏附分子、细胞因子等具有相同的核因子-κB基因启动位点,核因子-κB被激活后可介导这些因子过表达,从而加重心肌缺血再灌注后的炎症反应。本文就核因子-κB介导心肌缺血再灌注损伤机制的研究进展作一综述。

Inflammation plays a key role in myocardial ischemia reperfusion injury, which also involves the whole process of myocardial cell injury. The inflammatory response related adhesion molecules and cytokines have the same gene starting sites of nuclear faetor-κB. The activated nuclear factor-κB aggravates the inflammatory response after myocardial ischemia reperfusion by mediating the excessive expression of the above factors. This paper reviews the mechanism of myocardial ischemia-reperfusion injury mediated by nuclear factor-κB.