蛋白激酶B
神经保护
缺血
缺氧(环境)
免疫印迹
医学
缺血预处理
磷酸化
内分泌学
药理学
内科学
化学
神经科学
生物
细胞生物学
生物化学
氧气
基因
有机化学
作者
Lijun Zhan,Tao Wang,Wen Li,Zao C. Xu,Weiwen Sun,En Xu
标识
DOI:10.1111/j.1471-4159.2010.06816.x
摘要
J. Neurochem. (2010) 114 , 897–908. Abstract It is well established that pre‐conditioning protects neuronal injury against ischemia. However, the molecular mechanisms underlying ischemic tolerance are not completely understood. The purpose of the present study was to investigate the role of Akt/forkhead transcription factor, class O (FoxO) pathway in hypoxic pre‐conditioning (HPC) using a newly developed HPC to transient global cerebral ischemia (tGCI) model in adult rats. HPC for 30–120 min significantly reduced cell death in the CA1 subregion after 10 min of tGCI. HPC was effective only when applied 1–4 days before ischemia. The maximum protection was observed with 30 min of hypoxia and 1 day interval between hypoxia and ischemia. The phosphorylated Akt and FoxOs measured by western blot and immunohistochemistry were significantly increased after hypoxia‐ischemia except for a transient decrease in the HPC group. Lateral ventricular infusion of LY294002 before HPC blocked the increase in phosphorylated Akt and FoxOs and increased neuronal damage in HPC animals. These results suggest that pre‐exposure to hypoxia induces protection against tGCI in adult rats. Activation of Akt results in the inactivation of FoxOs which may mediate ischemic tolerance after HPC.
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