HO-1/CO系统在缺血/再灌注中的保护机制

缺血/再灌注(ischemia/reperfusion,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、休克以及器官移植导致器官功能和结构损伤的原因之一.在已知的I/R损伤的众多病理机制中已经明确氧化应激产生的活性氧自由基和炎症反应具有重要的作用.血色素氧合酶-1(heme oxygenase-1,HO-1)能催化血色素降解生成胆绿素、一氧化碳(carbon monoxide,CO),并释放Fe2+离子.近年来的研究已经证明HO-1及其催化产物CO具有抗氧化应激和抗炎作用,在正规损伤中能够发挥对组织器官的保护作用.现就I/R损伤中HO-1/CO系统的保护作用进行综合阐述.

Mechanism of protective effection of HO-1/CO system in ischemia/reperfusion

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. We summarize the currently available data regarding the role of the HO/CO system in the prevention of I/R injury.