2001年11月
Sublethal cerebral ischemia inhibits caspase-3 activation induced by subsequent prolonged ischemia in the C57black/Crj6 strain mouse
NEUROSCIENCE LETTERS
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- 巻
- 315
- 号
- 3
- 開始ページ
- 133
- 終了ページ
- 136
- 記述言語
- 英語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1016/S0304-3940(01)02368-0
- 出版者・発行元
- ELSEVIER SCI IRELAND LTD
Caspase-3 activation has been implicated in ischemic neuronal death. In the present study, we examined if cerebral ischemic tolerance induced by sublethal ischemia is associated with an attenuation of caspase-3 activation in a mouse forebrain ischemia model. Forebrain ischemia in C57Black/Crj6 strain mice was induced by bilateral common carotid artery occlusion (BCCAO) for 18 min. Two episodes of 6-min ischemia were carried out as preconditioning 48 and 72 h before the 18-min BCCAO. Caspase-3-like activity was determined by fluorescently monitoring the release of amino-4-methylcoumarin from N-acetyl-Asp-Glu-Val-Asp-7-amino-4-methylcoumarin in the striatal protein extracts at 4, 24, and 72 h after reperfusion. The results showed that the ischemic preconditioning significantly attenuated caspase-3 activation at 4, 24, and 72 h after reperfusion, and reduced neuronal loss caused by the 18-min ischemia as examined on the 7th day after reperfusion. The present results suggest that the neuroprotection achieved by ischemic preconditioning is related to an attenuation of caspase-3 activation. (C) 2001 Elsevier Science Ltd. All rights reserved.
- リンク情報
- ID情報
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- DOI : 10.1016/S0304-3940(01)02368-0
- ISSN : 0304-3940
- Web of Science ID : WOS:000172603100006