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作 者:海艇(综述)[1] 徐涛(审阅)[1] 王晓峰(审阅)[1]
机构地区:[1]北京大学人民医院泌尿外科,北京市100044
出 处:《医学分子生物学杂志》2010年第6期552-556,共5页Journal of Medical Molecular Biology
摘 要:器官移植术中及术后移植器官的缺血再灌注损伤(ischemia-repeffusion injury,IRI)和免疫排斥反应一直困扰着外科医生.血红素加氧酶-1(heme oxygenase-1,HO-1)是血红素代谢过程中的限速酶,广泛分布于哺乳动物的各种组织细胞中.血红素在它的催化下降解代谢为一氧化碳(CO)、胆绿素和游离铁离子.HO-1在氧化应激、炎性反应、低氧和缺血等状态下均能高度表达.HO-1及其催化血红素代谢产物主要通过抗炎性反应、抗氧化反应、调节同种异体反应性T细胞的活性及增殖、抗内皮细胞凋亡、抑制内皮细胞活化等作用机制,对移植器官起到抗IRI和抗免疫排斥作用,从而增加移植器官成活率及延长其存活时间.Organ transplantation has been used to treat many end-stage diseases for many years. However, until now, how to reduce ischemia-reperfusion injury and immunologic rejection are still problems bothering researchers. Heme oxygenase-1 (HO-1) an inducible isoform of HO, has been found in a series of cells in mammal animals. As the rate-limiting enzymes in heine metab- olism, HO-1 degrades heme to CO, biliverdin, and free divalent iron. Additionally, HO-1 can be up-regulated in response to oxidative stress, inflammation, hypoxia and ischemia. HO-1 and the corresponding heine metabolites may exert potent cellular protection, through anti-inflammatory, anti-oxidative stress, anti-apoptotic and endothelioeyte activation inhibition mechanisms. Therefore, the transplant organ survival may be enhanced.
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