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内皮素(endothelin,ET)是Yanagisawa首先从猪的主动脉内皮细胞中分离出来并命名,ET是至今所知道的最强力的内源性血管收缩剂[1],同时还有促进内皮细胞增殖的作用。ET-1主要来自血管内皮细胞,也可产生于平滑肌细胞、心肌细胞等其它细胞。缺血再灌注损伤(ischemia reperfusion in-jury)是指缺血组织或器官重获血流灌注或氧供后,对组织和器官所产生的损伤作用。近年来发现,缺血再灌注损伤与内皮素的作用有密切的联系,内皮素的作用可能在肾缺血再灌注损伤中起重要作用。本文从分子生物学水平将内皮素介导肾缺血-再灌注损伤的研究情况进行综述。
Endothelin (ET) is first isolated and named by Yanagisawa from porcine aortic endothelial cells. ET is the most potent endogenous vasoconstrictor known to date [1] and promotes endothelial cell proliferation Role. ET-1 mainly from vascular endothelial cells, can also be generated in smooth muscle cells, myocardial cells and other cells. Ischemia-reperfusion injury (ischemia-reperfusion in-jury) refers to the ischemic tissue or organ regained blood flow or oxygen supply, the damage to the tissues and organs. In recent years, it has been found that ischemia-reperfusion injury is closely related to the role of endothelin, and the role of endothelin may play an important role in renal ischemia-reperfusion injury. This review summarizes the progress of endothelin-mediated renal ischemia-reperfusion injury at molecular biology level.