HO-1CO系统在缺血再灌注中的保护机制.docVIP

HO-1/CO系统缺血再灌注重庆医科大学附属第一医院麻醉科 400016 刘力 闵苏 【摘要】 缺血再灌注(I/R)损伤是心肌梗死等许多疾病的病理生理基础，也是手术、创伤、休克器官移植器官功能和结构损伤的原因之一。缺血再灌注损伤的机制已经明确氧化应激产生的活性氧自由基具有重要的作用。血色素氧合酶(Heme oxygenase-1 HO-1)是催化血色素降解生成胆绿素carbon monoxide CO），并释放Fe2+离子。近的研究已经证明HO-1CO具有抗氧化应激和抗炎作用，在I/R损伤中组织器官保护作用。I/R损伤中HO-1/CO系统保护作用。 【关键词】 血红素氧合酶 一氧化碳 缺血再灌注 Mechanism HO-1/CO system protective effection in ischemia/reperfusion Li liu Su min (Department of Anesthesiology ,The First Affiliated Hospital of Chongqing Medical University) 【Abstract】 Ischemia/reperfusion (I/R) injury occurs frequently in a variety of clinical settings, including myocardial infarction, surgery, trauma,shock, and organ transplantation. Although the exact mechanisms involved in the pathogenesis of I/R injury have not been fully elucidated, it is generally believed that pro-inflammatory cytokines, and mediators generated in the setting of oxidative stress, such as reactive oxygen species (ROS), play important roles. Heme oxygenase (HO) is the rate-limiting enzyme that catalyzes the degradation of heme into equimolar quantities of biliverdinand carbon monoxide (CO), while the iron is released. HO-1, biliverdin, and CO, have been shown to possess generalized endogenous anti-inflammatory activities and provide protection against I/R injury. Further, recent observations have demonstrated that exogenous HO-1 expression, as well as exogenously administered CO have potent cytoprotective effects on I/R injury as well. we summarize the currently available data regarding the role of the HO/CO system in the prevention I/R injury. 【Key word】 Heme oxygenase carbon monoxide ischemia-reperfusion 缺血再灌注(I/R)损伤是在可逆的组织器官缺血损伤的基础上发展成为不可逆的细胞功能代谢障碍和结构破坏的病理生理过程。尽早恢复缺血组织的血流又防止再灌注损伤的发生是亟待解决的重要课题。近年来，对血色素氧合酶（Heme oxygenase HO）的研究日益受到人们的重视，其抗氧化应激；抗炎症；抗细胞凋亡作用被广泛的用于缺血再灌注损伤的研究，为许多疾病的诊疗和围术期组织器官的保护提供一个新的方向。 概述 血色素氧合酶（HO）是血红素代谢的限速酶，代谢生成胆绿素Fe2+、CO，参与机体抗氧化反应。HO有三类形式同工酶：HO-1，HO-2，HO-3[1]。HO-1在体内分布最为广泛，能够接受各种应激刺激缺氧、ROS、细胞因子、NO、重金属、紫外线A（320-380nm）、、过氧化氢硫氢基—SH）活性物质[]。CO是机体内重