细胞间黏附分子-1与肾缺血再灌注损伤  

ICAM-1 and renal ischmic-reperfusion injury

作　　者：邱振宇[1] 周盾[1] 

机构地区：[1]锦州医学院第一附属医院肾内科,辽宁锦州121001

出　　处：《基础医学与临床》2007年第1期100-104,共5页Basic and Clinical Medicine

摘　　要：细胞间黏附分子-1(ICAM-1)与肾脏缺血再灌注损伤的病理生理密切相关。肾缺血后损伤显示,损伤不仅是血供中断后组织缺氧的结果,更有再灌注进程中引起炎症反应的激活过程。浸润的白细胞在再灌注中起有害作用,其为活性氧自由基、蛋白水解酶及细胞因子的一个潜在来源。已有证据证实,ICAM-1在白细胞黏连、募集至炎症组织起关键作用。本文着重探讨ICAM-1在肾缺血再灌注损伤中的作用和意义。It has been well-documented that ICAM-1 implicates in pathophysiology of ischemic-reperfusion injury of the kidney. Renal injury after ischemia appears to be a consequence of tissue hypoxia not only from interrupted blood supply but also from the process of reperfusion which leads to an active inflammatory process. Infiltrating leukocytes are potential source of reactive oxygen species. Proteolytic enzymes and cytokines, which during reperfusion may play a detrimental role. It has been suggested that ICAM-1 plays a key role during leukocyte adhesion and recruitment to inflamed tissue. The goal of the review is to explore the effect and significance of ICAM-1 as well as its mechanism in renal ischemia-reperfunsion.

关 键 词：细胞间黏附分子-1 缺血再灌注损伤 肾 

分 类 号：R692[医药卫生—泌尿科学] R363[医药卫生—外科学]