肝脏缺血/再灌注损伤与细胞凋亡研究进展  

Research Progresses of Hepatic Ischemia Reperfusion Injury and Apoptosis

作　　者：王强[1] 梁志鹏[1] 

机构地区：[1]广东医学院附属湛江中心人民医院肝胆外科

出　　处：《医学综述》2009年第7期990-993,共4页Medical Recapitulate

摘　　要：肝脏缺血／再灌注损伤是肝脏缺血／再灌注后肝脏功能障碍和结构损伤加重的现象。研究表明，细胞凋亡是肝脏缺血／再灌注损伤的重要机制之一，其机制与各种活性氧的生成、线粒体通透性的改变、内质网应激和钙超载等有关，同时还受一些基因的调控。本文就肝脏缺血／再灌注损伤时细胞凋亡的发生机制和基因调控予以综述。Hepatic ischemia reperfusion injury （HIRI） is the aggravation of liver function or structure damages after hepatic ischemia reperfusion. Some studies have showed apoptosis might be one of the crucial mechanisms of hepatic ischemia reperfusion injury, which is associated with production of reactive oxygen species, mitochondrial permeability transition, endoplasmic reticulum stress and calcium overload. Apoptosis is controlled by some genes. This article reviewed the mechanisms and gene modulation of apoptosis during HIRI.

关 键 词：再灌注损伤 细胞凋亡 基因 肝脏 

分 类 号：R363[医药卫生—病理学]