Chan P H
Department of Neurosurgery, University of California, San Francisco 94143.
Brain Pathol. 1994 Jan;4(1):59-65. doi: 10.1111/j.1750-3639.1994.tb00811.x.
Oxygen free radicals have been widely implicated in the pathogenesis of brain injury due to ischemia followed by reperfusion. The success of making transgenic animals overexpressing human CuZn-superoxide dismutase (CuZn-SOD) in brain cells allows researchers to discern the specific role of superoxide radicals in reperfusion injury after focal ischemia. It has been shown that increased brain levels of CuZn-SOD in transgenic mice protect neurons from ischemia/reperfusion injury. However, overexpression of CuZn-SOD does not provide neuronal protection in permanent focal ischemia in mice, when compared with non-transgenic mouse littermates. It is proposed that molecular genetic approaches of modifying antioxidant levels in the brain offer a unique tool for studying oxidative mechanisms in focal cerebral ischemia.
氧自由基在缺血后再灌注所致脑损伤的发病机制中具有广泛影响。成功培育出在脑细胞中过度表达人铜锌超氧化物歧化酶(CuZn-SOD)的转基因动物,使研究人员能够辨别超氧自由基在局灶性缺血后再灌注损伤中的具体作用。研究表明,转基因小鼠脑中CuZn-SOD水平升高可保护神经元免受缺血/再灌注损伤。然而,与非转基因同窝小鼠相比,CuZn-SOD的过度表达在小鼠永久性局灶性缺血中并不能提供神经元保护。有人提出,改变脑中抗氧化剂水平的分子遗传学方法为研究局灶性脑缺血的氧化机制提供了一个独特的工具。