环孢素A在心肌缺血再灌注损伤中的心脏保护作用研究进展

Cardioprotective Effects of Cyclopsporine A in Treatment of Myocardial Reperfusion Injury

越来越多的证据显示线粒体通透性转换孔(mPTP)的开放在心肌缺血再灌注损伤中发挥着关键作用。尽管其结构仍不明确,但亲环素D却是其主要的组成成分之一。环孢素A是一种有效的免疫抑制剂,可结合于线粒体亲环素D,从而抑制mPTP的开放。许多动物实验及部分小规模临床研究表明,其可以通过抑制mPTP而减少心肌梗死面积。然而,也有研究提示环孢素A并没有心脏保护作用。现就环孢素A在心肌缺血再灌注损伤中可能的心脏保护作用机制、相关的动物实验模型及临床研究、可能的影响因素及进一步研究方向进行综述。

Accumulating evidence suggests that the opening of the mitochondrial permeability transition pore（ mPTP） plays a key role in myocardial reperfusion injury. Its structure is still not clearly defined but one of its key components is the protein cyclophilin D. Cyclosporine A,which has potent immunosuppressor activity,can bind to the mitochondrial cyclophilin D and thereby inhibit the mPTP from opening. Cyclosporine A has been shown to reduce infarct size in various experimental conditions and some clinical studies by inhibiting the opening of mPTP,although similar studies have been done with negative results. In this article,the potential mechanisms,experimental and clinical studies,probable influential factors,and future research of the cardioprotective effects of cyclosporine A in myocardial reperfusion injury have been reviewed.