Reduction of copper,zinc-superoxide dismutase in knockout mice does not affect edema or infarction volumes and the early release of mitochondrial cytochrome c after permanent focal cerebral ischemia
Reduction of copper,zinc-superoxide dismutase in knockout mice does not affect edema or infarction volumes and the early release of mitochondrial cytochrome c after permanent focal cerebral ischemia
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DOI：
10.1016/s0006-8993(00)03134-6
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发表时间：
2001-01-19
期刊：
影响因子：
2.9
通讯作者：
Chan, PH
中科院分区：
文献类型：
--
作者：
Fujimura, M;Morita-Fujimura, Y;Chan, PH
铜锌超氧化物歧化酶（SOD 1）被证明是高度保护脑缺血/再灌注损伤。我们最近报道，SOD 1阻止释放线粒体细胞色素c和随后的细胞凋亡后缺血/再灌注小鼠。为了研究其对永久性局灶性脑缺血的剂量依赖性作用，我们检查了SOD 1敲除突变体（Sod 1-/+和Sod 1-/-）和野生型同窝仔在局灶性脑缺血24小时后的神经功能缺损评分、梗死体积和半球扩大量。我们还研究了缺血后细胞色素c的释放和随后的DNA片段化。在神经功能缺损评分、梗死体积和水肿形成方面无差异。脑缺血2 h细胞色素c含量和24 h DNA断裂量无明显变化。结果表明，SOD 1酶似乎不影响脑梗死、脑水肿，也不影响在没有再灌注损伤的永久性局灶性脑缺血后细胞凋亡的线粒体信号通路。(C)2001 Elsevier Science B. V.保留所有权利。
Copper,zinc-superoxide dismutase (SOD1) was shown to be highly protective against ischemia/reperfusion injury in the brain. We have recently reported that SOD1 prevents the release of mitochondrial cytochrome c and subsequent apoptosis after ischemia/reperfusion in mice. To investigate its dose dependent effect on permanent focal cerebral ischemia, we examined neurological deficit scores, infarction volume, and the amount of hemisphere enlargement after 24 h of focal cerebral ischemia in both knockout mutants of SOD1 (Sod1 -/+ and Sod1 -/-) and wild-type littermates. We also examined the release of cytochrome c and subsequent DNA fragmentation after ischemia. There were no differences in the neurological deficit scores, infarction volumes and edema formation. There was also no difference of the amount cytosolic cytochrome c at 2 h and of the amount of DNA fragmentation at 24 h after focal cerebral ischemia. The results indicate that the SOD1 enzyme does not appear to affect cerebral infarction, cerebral edema nor the mitochondrial signaling pathway for apoptosis following permanent focal cerebral ischemia where there is no reperfusion injury. (C) 2001 Elsevier Science B.V. All rights reserved.