Journal of Veterinary Medical Science
Online ISSN : 1347-7439
Print ISSN : 0916-7250
ISSN-L : 0916-7250
Anatomy
Melatonin Attenuates the Cerebral Ischemic Injury via the MEK/ERK/p90RSK/Bad Signaling Cascade
Phil-Ok KOH
著者情報
キーワード: ERK, MEK, Melatonin, Neuroprotection, p90RSK
ジャーナル フリー

2008 年 70 巻 11 号 p. 1219-1223

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抄録

Melatonin prevents neuronal cell death in ischemic brain injury. This study investigated whether melatonin inhibits the apoptotic signal through the activation of Raf-MEK-ERK and its downstream targets, including 90 ribosomal S6 kinase (p90RSK) and Bad. Adult male rats were treated with melatonin (5 mg/kg) or vehicle prior to middle cerebral artery occlusion (MCAO). Brains were collected 24 hr after MCAO. We confirmed that melatonin significantly decreases the number of TUNEL positive cells in the cerebral cortex. Western blot analysis showed that levels of Raf-1, MEK1/2, and ERK1/2 phosphorylation decrease in vehicle-treated animals. Melatonin prevents the injury-induced decrease of Raf-1, MEK1/2, and ERK1/2 phosphorylation. Also, it inhibits the injury-induced decrease of p90RSK and Bad phosphorylation. Recently, we reported that melatonin prevents the injury-induced reduction of interaction between pBad and 14-3-3 and inhibits the activation of caspase-3. Subsequently, melatonin prevents the injury-induced an increase of cleaved PARP levels. Taken together, these results suggest that melatonin prevents cell death resulting from ischemic brain injury, and that its neuroprotective effects are mediated by the activation of Raf/MEK/ERK/p90RSK cascade.

著者関連情報
© 2008 by the Japanese Society of Veterinary Science

この記事はクリエイティブ・コモンズ [表示 - 非営利 - 改変禁止 4.0 国際]ライセンスの下に提供されています。
https://creativecommons.org/licenses/by-nc-nd/4.0/deed.ja
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