Neuroprotective effect of an antioxidant in ischemic brain injury - Involvement of neuronal apoptosis
Neuroprotective effect of an antioxidant in ischemic brain injury - Involvement of neuronal apoptosis
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DOI：
10.1385/ncc:2:1:059
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发表时间：
2005-01-01
影响因子：
3.5
通讯作者：
Chan, PH
中科院分区：
文献类型：
--
作者：
Fujimura, M;Tominaga, T;Chan, PH
活性氧（reactive oxygen species，ROS）的产生与脑缺血再灌注损伤有关，抗氧化酶被认为是脑缺血后细胞对抗ROS有害作用的主要机制之一。ROS还介导可能导致脑缺血后细胞凋亡的线粒体信号通路。最近的发展和可用性的转基因和敲除突变的啮齿动物，无论是过度表达或缺乏抗氧化基因，提供了强大的工具，解剖的分子和细胞机制的信号通路，直接氧化损伤，或两者都参与缺血性脑损伤。本文着重于ROS或抗氧化系统的贡献，缺血后细胞凋亡的分子途径短暂性局灶性脑缺血，使用转基因小鼠过表达的胞质抗氧化剂铜/锌超氧化物歧化酶。
The production of reactive oxygen species (ROS) has been implicated in reperfusion injury after cerebral ischemia, and antioxidant enzymes are believed to be among the major mechanisms by which the cells counteract the deleterious effect of ROS after cerebral ischemia. ROS also mediate the mitochondrial signaling pathway that may lead to apoptosis following cerebral ischemia. The recent development and availability of transgenic and knockout mutant rodents that either overexpress or are deficient in antioxidant genes have provided powerful tools for dissecting the molecular and cellular mechanisms of signaling pathways, direct oxidative damage, or both that are involved in ischemic brain injury. This article focuses on the contribution of ROS or an antioxidant system to the molecular pathway of postischemic apoptosis following transient focal cerebral ischemia by using transgenic mice that overexpress the cytosolic antioxidant copper/zinc superoxide dismutase.