大脑中动脉闭塞后大鼠黑质锰超氧化物歧化酶的免疫组化观察

An immunohistochemical observation of manganese superoxide dismutase in rat substantia nigra after occlusion of middle cerebral artery.

作者信息

Liu X H, Kato H, Araki T, Itoyama Y, Kato K, Kogure K

机构信息

Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.

出版信息

Neurosci Lett. 1994 May 23;173(1-2):103-6. doi: 10.1016/0304-3940(94)90159-7.

DOI:10.1016/0304-3940(94)90159-7

PMID:7936392

Abstract

We investigated immunohistochemically the localization and changes of manganese superoxide dismutase (Mn-SOD) in substantia nigra after 1 h of middle cerebral artery (MCA) occlusion in the rat with reperfusion periods of 1, 3, 7, and 14 days. In normal rats, Mn-SOD immunoreactivity was observed intensely in many large neurons in substantia nigra pars reticulata (SNr) and weakly in neurons in the pars compacta (SNc). The immunoreactivity of the neurons in both SNr and SNc was reduced after 1 day and almost lost 3 days after MCA occlusion, although these neurons showed completely normal morphology. The immunoreactivity recovered only in the large neurons in SNr from the 7th day and well preserved after 2 weeks, when SNr showed obvious atrophy. The results indicate that oxidative stress may be involved in the pathogenesis of the secondary postischemic neurodegeneration in SN.

摘要

我们采用免疫组织化学方法，研究了大鼠大脑中动脉（MCA）闭塞1小时后再灌注1、3、7和14天，黑质中锰超氧化物歧化酶（Mn-SOD）的定位及变化情况。在正常大鼠中，在黑质网状部（SNr）的许多大神经元中观察到强烈的Mn-SOD免疫反应性，而在致密部（SNc）的神经元中则较弱。MCA闭塞1天后，SNr和SNc中神经元的免疫反应性均降低，且在MCA闭塞3天后几乎消失，尽管这些神经元的形态完全正常。从第7天开始，免疫反应性仅在SNr的大神经元中恢复，2周后保存良好，此时SNr出现明显萎缩。结果表明，氧化应激可能参与了SN缺血后继发性神经退行性变的发病机制。