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在永久性局灶性脑缺血后,超氧化物歧化酶-1转基因小鼠的脑梗死面积并未减小。

Brain infarction is not reduced in SOD-1 transgenic mice after a permanent focal cerebral ischemia.

作者信息

Chan P H, Kamii H, Yang G, Gafni J, Epstein C J, Carlson E, Reola L

机构信息

Department of Neurology, University of California, School of Medicine, San Francisco 94143-0114.

出版信息

Neuroreport. 1993 Dec 13;5(3):293-6. doi: 10.1097/00001756-199312000-00028.

Abstract

Using a mouse model with intraluminal blockade of the middle cerebral artery (MCA) which produced both cortical and striatal infarction, the effect that superoxide radicals have on cerebral infarction, local cerebral blood flow, and neurological deficits after 24 h of permanent focal cerebral ischemia in transgenic mice (Tg) overexpressing human CuZn-superoxide dismutase (SOD-1) was examined. There were no difference between SOD-1 Tg mice and non-Tg littermates observed in the infarct areas of brain slices, the infarct volume, the local cerebral blood flow, or the neurological deficits. These data suggest that pre-existing high levels of antioxidant enzyme failed to provide neuronal protection against permanent focal cerebral ischemia.

摘要

利用一种大脑中动脉(MCA)腔内阻塞的小鼠模型,该模型会导致皮质和纹状体梗死,研究了超氧自由基对过表达人铜锌超氧化物歧化酶(SOD-1)的转基因小鼠(Tg)永久性局灶性脑缺血24小时后脑梗死、局部脑血流量和神经功能缺损的影响。在脑切片梗死面积、梗死体积、局部脑血流量或神经功能缺损方面,未观察到SOD-1转基因小鼠与非转基因同窝小鼠之间存在差异。这些数据表明,预先存在的高水平抗氧化酶未能为神经元提供针对永久性局灶性脑缺血的保护作用。

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