内源性抗氧化应激机制在缺血预处理与缺血再灌注损伤中的研究进展

doi:10.3969/j.issn.2095-1396.2016.02.008

神经药理学报 ›› 2016, Vol. 6 ›› Issue (2): 46-52.DOI: 10.3969/j.issn.2095-1396.2016.02.008

内源性抗氧化应激机制在缺血预处理与缺血再灌注损伤中的研究进展

王欢欢，薛茜，邹玉安

1. 河北北方学院，张家口，075000，中国
2. 河北北方学院第一附属医院神经内科，张家口，075000，中国

出版日期:2016-04-26 发布日期:2016-05-10
通讯作者: 薛茜，女，教授，硕士，研究生导师；研究方向：神经内科临床方向；E-mail：xueqian6166@163.com 邹玉安，男，教授，硕士，研究生导师；研究方向：神经药理学；E-mail：zya8857111@sohu.com
作者简介:王欢欢，女，硕士研究生；研究方向：缺血性脑血管病研究；E-mail：1271643589@qq.com
基金资助:
河北省医学科学研究重点课题（No.20150054）

Research Progress of the Mechanism of Endogenous Antioxidant Stress in Cerebral Ischemic Preconditioning and Ischemia Reperfusion Injury

WANG Huan-huan，XUE Qian，ZOU Yu-an

1. Hebei North University，Zhangjiakou，075000，China
2. Department of Neurology，the First Affiliated Hospital of Hebei North University，Zhangjiakou，075000，China

Online:2016-04-26 Published:2016-05-10
Contact: 薛茜，女，教授，硕士，研究生导师；研究方向：神经内科临床方向；E-mail：xueqian6166@163.com 邹玉安，男，教授，硕士，研究生导师；研究方向：神经药理学；E-mail：zya8857111@sohu.com
About author:王欢欢，女，硕士研究生；研究方向：缺血性脑血管病研究；E-mail：1271643589@qq.com
Supported by:
河北省医学科学研究重点课题（No.20150054）

摘要/Abstract

摘要： 脑缺血预处理是指给予脑组织一个低于阈值的缺血缺氧刺激，激活机体的内源性保护因子或信号通路，从而产生脑缺血耐受的现象。预处理涉及的神经保护机制包括抗凋亡、抗氧化应激、抑制炎症反应、调节兴奋性/ 抑制性神经递质、血管重塑、保护血脑屏障、维持能量代谢/ 线粒体膜电位以及激活DNA 修复和自我修复等作用。而氧化应激损伤、自由基连锁反应是缺血再灌注损伤的核心病理环节，该文对内源性抗氧化应激机制在缺血预处理引起的再灌注损伤中作用进行综述，为缺血缺氧性脑病的临床治疗提供理论依据。

关键词: 脑缺血预处理, 缺血再灌注, 内源性抗氧化应激, 信号通路

Abstract: Cerebral ischemic preconditioning （CIP） induced by sublethal transient cerebral ischemia could increase the tolerance of the brain tissue to subsequent lethal ischemia by activating the endogenous protective factor or signaling pathways. Establishing such a tolerance involved multiple mechanisms：resistance to apoptosis，antioxidant stress，inhibiting the inflammatory response，adjusting the excitatory and inhibitory neurotransmitter，vascular remodeling，protecting blood brain barrier，maintaining energy metabolism and mitochondrial membrane potential and activating the DNA repair and self-repair etc. However，oxidative stress damaging，free radical chain reacting is the core of ischemia-reperfusion injury. Therefore，a better understanding of the mechanism of cerebral ischemic preconditioning and endogenous antioxidant stress in the ischemia reperfusion injury could provide theoretical basis for clinical treatment of ischemia anoxic encephalopathy.

Key words: cerebral ischemic preconditioning, ischemia reperfusion injury, endogenous antioxidant stress, signaling pathways

中图分类号:

R964

王欢欢, 薛茜, 邹玉安. 内源性抗氧化应激机制在缺血预处理与缺血再灌注损伤中的研究进展[J]. 神经药理学报, 2016, 6(2): 46-52.

WANG Huan-huan, XUE Qian, ZOU Yu-an. Research Progress of the Mechanism of Endogenous Antioxidant Stress in Cerebral Ischemic Preconditioning and Ischemia Reperfusion Injury[J]. ACTA NEUROPHARMACOLOGICA, 2016, 6(2): 46-52.

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内源性抗氧化应激机制在缺血预处理与缺血再灌注损伤中的研究进展

Research Progress of the Mechanism of Endogenous Antioxidant Stress in Cerebral Ischemic Preconditioning and Ischemia Reperfusion Injury

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