Neuroprotection by dehydroepiandrosteronesulfaterole of an NFκB‐like factor
作者:
Xianrong Mao,
Steven Barger,
期刊:
NeuroReport
(OVID Available online 1998)
卷期:
Volume 9,
issue 4
页码: 759-763
ISSN:0959-4965
年代: 1998
出版商: OVID
关键词: Cell culture;DHEA;Excitotoxicity;Hippocampus;N FκB
数据来源: OVID
摘要:
LEVELS of dehydroepiandrosterone (DHEA) and its sulfated derivative (DHEA-S) decline during aging and reach even lower levels in Alzheimer's disease (AD). Previously published effects of DHEA and DHEA-S on unchallenged neuronal survival led us to test them in an excitotoxicity paradigm. While DHEA-S protected hippocampal neurons against glutamate, little protection was observed with equivalent doses of DHEA itself. This differential neuroprotection was consistent with the ability of DHEA-S (but not DHEA) to elevate a κB-dependent transcription factor activity, a phenomenon we previously have connected with neuroprotection. Furthermore, suppression o fκB DNA-binding by ‘decoy’ oligonucleotides blocked the neuroprotective activity of DHEA-S. These findings imply that age-related declines in the availability of DHEA-S could exacerbate neurotoxicity, and the data suggest that therapeutic gains may be obtained with pharmacological manipulation o fκB-dependent transcription in neurons.
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