国际麻醉学与复苏杂志   2011, Issue (6): 2-2
    
缺血后处理与线粒体通透性转运孔
张维亮, 赵砚丽1()
1.河北省人民医院麻醉科
Ischemic postconditioning and Mitochondrial permeability transition pore
 全文:
摘要:

概述 缺血后处理(ischemic postconditioning,IPo)能明显减轻器官缺血再灌注损伤,动物实验和临床研究均已经得到证实,其机制可能与增强组织抗氧化能力和抑制细胞凋亡有关。然而近些年提出线粒体通透性转换孔(mitochondrial permeability transition pore,MPTP)在IPo减轻器官缺血再灌注损伤研究中发挥重要作用。现将从MPTP的角度探讨IPo的保护机制。目的 阐述MPTP在IPo器官保护机制中的作用。内容 MPTP是IPo发挥作用的最终靶点。它是位于线粒体内外膜上的复合蛋白孔道,其开放程度与细胞钙离子超载、线粒体膜电位降低、氧活性物质增多、凋亡蛋白释放等关系密切。IPo可通过多条信号转导途径发挥器官保护作用,对MPTP的调节是其重要方面。趋向 MPTP的研究完善了IPo器官保护机制。

关键词: 线粒体通透性转换孔;缺血后处理;线粒体ATP敏感性钾通道;
Abstract:

Summary Ischemic postconditioning alleviating ischemia reperfusion injury had been confirmed by experimental study and clinical study,the mechanism was relevantd to enhancing organization antioxidant capacity and Inhibiting apoptosis.However,in recent years,it had putted forward that mitochondrial permeability transition pore play a important role in ischemic postconditioning alleviating ischemia reperfusion injury, This review will discuss the mechanisms of ischemic postconditioning from Mitochondrial permeability transition pore.Purpose It elaborates the role of MPTP in IPo organs protection mechanism.Content Mitochondrial permeability transition pore,(MPTP)is identified as the final targets of ischemic postconditioning.It is a kind of composite protein channel located inside and outside on the mitochondrial membranes, which’s open induced intracellular calcium overload,the mitochondrial membrane potential reduced,reactive oxygen species increased, pro-apoptotic proteins released.IPo attenuates reperfusion injury by several signal transduction pathways, and regulation of Mitochondrial permeability transition pore is an important aspect.Trend The MPTP research perfect the IPo organs protection mechanism.

Key words: Mitochondrial permeability transition pore; Mitochondrial KATP channel; Ischemic postconditioning