阿司匹林可降低大鼠脑匀浆中氰化物诱导的自由基产生和脂质过氧化反应。

Cyanide-induced free radical production and lipid peroxidation in rat brain homogenate is reduced by aspirin.

作者信息

Daya S, Walker R B, Anoopkumar-Dukie S

机构信息

Faculty of Pharmacy, Rhodes University, Grahamstown, South Africa.

出版信息

Metab Brain Dis. 2000 Sep;15(3):203-10. doi: 10.1007/BF02674529.

DOI:10.1007/BF02674529

PMID:11206589

Abstract

The neuroprotective properties of aspirin were investigated using cyanide-induced neurotoxicity as model. Cyanide, a known neurotoxic agent significantly increased lipid peroxidation and superoxide anion levels in rat brain homogenate in a concentration-dependent manner (0.25-1.0 mM). When homogenate, containing 1.0 mM KCN was co-treated with aspirin (1.0 mM) there was a significant decrease in lipid peroxidation. Aspirin (0.5 mM and 1.0 mM) also significantly reduced KCN-induced superoxide anion generation. The results of the present report therefore indicate a neuroprotective role for aspirin.

摘要

以氰化物诱导的神经毒性为模型研究了阿司匹林的神经保护特性。氰化物是一种已知的神经毒性剂，它能以浓度依赖性方式（0.25 - 1.0 mM）显著增加大鼠脑匀浆中的脂质过氧化和超氧阴离子水平。当含有1.0 mM氰化钾的匀浆与阿司匹林（1.0 mM）共同处理时，脂质过氧化显著降低。阿司匹林（0.5 mM和1.0 mM）也显著减少了氰化钾诱导的超氧阴离子生成。因此，本报告结果表明阿司匹林具有神经保护作用。