线粒体Sirt3活化在重症失血性休克发展进程中的作用  

Role of mitochondrial Sirt3 activation during severe hemorrhagic shock

作　　者：王齐 赵自刚[1] 牛春雨[1] Wang Qi;Zhao Zi-Gang;Niu Chun-Yu(Institute of Microcirculation,Hebei North University,Zhangjiakou 075000,China)

机构地区：[1]河北北方学院微循环研究所,河北张家口075000

出　　处：《中国急救医学》2018年第11期1005-1008,共4页Chinese Journal of Critical Care Medicine

基　　金：河北省自然科学基金（H2015405041）

摘　　要：Sirt3作为线粒体的一种去乙酰化酶，通过调节多种分子的去乙酰化，可缓解重症失血性休克发展过程中发生的血管低反应性、血管高通透性，降低氧化应激，抑制细胞坏死与凋亡，减轻线粒体损伤，发挥组织与细胞保护作用。本文综述Sirt3活化在重症失血性休克发展进程中的作用，希望针对Sirt3为防治重症失血性休克提供新的思路。Sirtuin 3 （Sirt3） is a mitochondrial enriched deacetylase. Activation of Sire3, which deacetylates transcription factors and cofactors, attenuates the severe hemorrhagic shock - induced vascular hypo - reactivity and vascular hyper - permeability, suppresses the injury of oxidative stress, inhibits cell necrosis and apoptosis, and alleviates the mitochondria damage and dysfunction, as a result, plays protective effects for tissues and cells. This review focuses on new data linking the activation of Sirt3 to management of severe hemorrhagic shock, and provides a novel implication for treatment of severe hemorrhagic shock.

关 键 词：Sirt3 失血性休克 血管反应性 血管通透性 氧化应激 

分 类 号：R605.971[医药卫生—急诊医学]