脂质过氧化抑制剂可保护培养的神经元免受氰化物诱导的损伤。

Inhibitors of lipid peroxidation protect cultured neurons against cyanide-induced injury.

作者信息

Müller U, Krieglstein J

机构信息

Institut für Pharmakologie und Toxikologie, Fachbereich Pharmazie und Lebensmittelchemie, Philipps-Universität, Marburg, Germany.

出版信息

Brain Res. 1995 Apr 24;678(1-2):265-8. doi: 10.1016/0006-8993(95)00196-w.

DOI:10.1016/0006-8993(95)00196-w

PMID:7620895

Abstract

We tested the 21-aminosteroid U-74500A and the 2-methylaminochroman U-83836E, two potent inhibitors of lipid peroxidation, for their protective efficacy against cyanide- or Fe2+/Fe(3+)-induced damage of cultured neurons from chick embryo telencephalon. U-74500A (0.1-10 microM) as well as U-83836E (0.01-10 microM) reduced cyanide-induced neurotoxicity, indicating that lipid peroxidation plays an important role in the genesis of cyanide-induced neuronal injury. Both U-74500A and U-83836E, but not the NMDA antagonist dizocilpine (1 microM, prevented Fe2+/Fe(3+)-induced neuronal degeneration.

摘要

我们测试了两种强效脂质过氧化抑制剂——21-氨基类固醇U-74500A和2-甲基氨基苯并二氢吡喃U-83836E，针对氰化物或Fe2+/Fe(3+)诱导的鸡胚端脑培养神经元损伤的保护效果。U-74500A（0.1 - 10微摩尔）以及U-83836E（0.01 - 10微摩尔）可减轻氰化物诱导的神经毒性，这表明脂质过氧化在氰化物诱导的神经元损伤发生过程中起重要作用。U-74500A和U-83836E均可减轻Fe2+/Fe(3+)诱导的神经元变性，但NMDA拮抗剂地佐环平（1微摩尔）则不能。