Dehydroepiandrosterone (DHEA) protects hippocampal cells from oxidative stress-induced damage

被引:207
|
作者
Bastianetto, S
Ramassamy, C
Poirier, J
Quirion, R
机构
[1] McGill Univ, Douglas Hosp, Res Ctr, Dept Psychiat, Verdun, PQ H4H 1R3, Canada
[2] Douglas Hosp, McGill Ctr Studies Aging, Verdun, PQ H4H 1R3, Canada
来源
MOLECULAR BRAIN RESEARCH | 1999年 / 66卷 / 1-2期
基金
英国医学研究理事会;
关键词
neurosteroid; antioxidant; free radical; neuroprotection; Alzheimer's disease;
D O I
10.1016/S0169-328X(99)00002-9
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
It has been postulated that decreases in plasma levels of dehydroepiandrosterone (DHEA) may contribute to the development of some age-related disorders. Along with neuroprotective and memory enhancing effects, DHEA has been shown to display antioxidant properties. Moreover, oxidative stress is known to cause lipid peroxidation and degenerative changes in the hippocampus, an area involved in memory processes and especially afflicted in Alzheimer's disease (AD). Accordingly, we investigated the antioxidant effects of DHEA in models of oxidative stress using rat primary hippocampal cells and human hippocampal tissue from AD patients and age-matched controls. A pre-treatment of rat primary mixed hippocampal cell cultures with DHEA (10-100 mu M) protected against the toxicity induced by H2O2 and sodium nitroprusside. Moreover, DHEA (10-100 mu M) was also able to prevent H2O2/FeSO4-stimulated lipid oxidation in both control and AD hippocampal tissues. Taken together, these data suggest that DHEA may be useful in treating age-related central nervous system diseases based on its protective effects in the hippocampus. (C) 1999 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:35 / 41
页数:7
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