Fujimura Miki, Tominaga Teiji, Chan Pak H
Department of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Japan.
Neurocrit Care. 2005;2(1):59-66. doi: 10.1385/NCC:2:1:059.
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.
活性氧（ROS）的产生与脑缺血后的再灌注损伤有关，抗氧化酶被认为是细胞对抗脑缺血后ROS有害作用的主要机制之一。ROS还介导了线粒体信号通路，这可能导致脑缺血后细胞凋亡。最近，转基因和基因敲除突变啮齿动物的发展和应用，这些动物要么过表达抗氧化基因，要么缺乏抗氧化基因，为剖析参与缺血性脑损伤的信号通路、直接氧化损伤或两者的分子和细胞机制提供了强大的工具。本文通过使用过表达胞质抗氧化铜/锌超氧化物歧化酶的转基因小鼠，重点研究了ROS或抗氧化系统对短暂性局灶性脑缺血后缺血性凋亡分子途径的作用。
