《中国康复理论与实践》

《中国康复理论与实践》 ›› 2010, Vol. 16 ›› Issue (12): 1140-1143.

• 论文 • 上一篇    下一篇

脑缺血再灌注后神经细胞凋亡机制及药物保护作用的研究进展

汪莹1，许栋明2，王文1，高东明3，张丽1，艾厚喜1，李林1   

  1. 1.首都医科大学宣武医院，北京市 100053；2.科技部火炬高新技术产业开发中心，北京市 100038；3.辽宁医学院，辽宁锦州市 121000。
  • 收稿日期:2010-10-13 修回日期:1900-01-01 出版日期:2010-12-25 发布日期:2010-12-25
  • 通讯作者: 王文

Advance in Apoptosis Mechanism on Nerve Cell after Cerebral Ischemia-reperfusion and Neuroprotective Drugs (review)

WANG Ying, XU Dong-ming, WANG Wen, et al   

  1. Xuanwu Hospital of Capital Medical University, Beijing 100053, China; Torch High Technology Industry Development Center, The Ministry of Science and Technology of the P.R.C., Beijing 100038, China; Department of Physiology, Liaoning Medical College, Jinzhou 121000, Liaoning, China
  • Received:2010-10-13 Revised:1900-01-01 Published:2010-12-25 Online:2010-12-25

PDF (PC)

被引次数

48

摘要： 脑缺血再灌注导致神经元损伤，凋亡相关基因及蛋白被激活，与此同时机体内释放大量的细胞因子诱发凋亡发生。目前研究表明，脑缺血再灌注后神经细胞凋亡的主要机制为线粒体损伤、钙超载及氧自由基的累积等。通过对以上机制的深入研究有助于开发新的脑保护药物，并进一步明确各种脑保护药物的治疗靶点和疗效。

关键词: 缺血再灌注, 神经细胞凋亡, 药物, 综述

Abstract: Cerebral ischemia-reperfusion results in damage on neuron, leading to genes and proteins related to apoptosis activation. At the same time, generous cytokines released after cerebral ischemia-reperfusion can induce the apoptosis of the neuron. Many current studies have showed that the major damage mechanisms on apoptosis of the neuron are mitochondrion impairment, calcium overload, increased levels of oxygen radicals and so on. The advance research on the mechanism contributes to explore new neuroprotective drugs, and further identify the target and therapeutic effect of drug treatment.

Key words: ischemia-reperfusion, apoptosis, drug, review