ASIA unversity:Item 310904400/16401
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    題名: Role of ERK Signaling in the Neuroprotective Efficacy of Magnesium Sulfate Treatment During Focal Cerebral Ischemia in the Gerbil Cortex
    作者: 黃志揚;HUANG, CHIH-YANG;Liou, Yi-Fan;Chung, Shu-Ying;Lin, Wen-Yuan;Jong, Gwo-Ping;Kuo, Chia-Hua;Tsai, Fuu-Jen;Cheng, Yi-Chang;Cheng, Fu-Chou;Lin, Jing-Ying
    貢獻者: 生物科技學系
    關鍵詞: magnesium sulfate;ERK, CREB;Bcl-2 family;mitochondria;focal cerebral ischemia
    日期: 2010-02
    上傳時間: 2012-11-23 09:12:35 (UTC+0)
    摘要: "Magnesium sulfate (MgSO4
    ) ameliorates focal ischemia-induced neuronal death in the rat and
    gerbil models. However, the molecular mechanisms for this neuroprotection are not known. Focal
    cerebral ischemia was produced by unilateral occlusion of the right common carotid artery and the right
    middle cerebral artery (CCAO + MCAO) for 30 min or 60 min. Treatment with MgSO4
    significantly
    increased the level of mitogen-activated protein kinase/extra-cellular signal-regulated kinase kinase 1/
    2 (MEK1/2), extra-cellular signal-regulated kinase 1/2 (ERK1/2), cyclic-AMP response element binding
    protein (CREB) phosphorylation and the anti-apoptotic protein Bcl-2 both in the non-ischemic (contralateral) and ischemic (ipsilateral) cortex. However, these effects were reversed by administration of
    U0126, a MEK kinase inhibitor. In the ipsilateral cortex, a significant increase in the level of the proapoptotic proteins Bax, Bad, BNIP3 and activated caspase 3 were detected at the end of focal ischemia
    compared to the non-ischemic cortex. Treatment of MgSO4
    prevented these ischemia-induced activations
    of the death cascade. Collectively, these data indicate that the ERK-CREB-Bcl-2 signaling pathway
    might be involved in MgSO4
    -induced neuroprotection following focal ischemia. Moreover, MgSO4
    treatment also resulted in a reduction in pro-apoptotic proteins. These results enhance our understanding
    on the role of MgSO4
    in treating cerebral ischemia."
    關聯: CHINESE JOURNAL OF PHYSIOLOGY
    顯示於類別:[生物科技學系] 期刊論文

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