Involvement of Akt/CREB signaling pathways in the protective effect of EPA against interleukin-1β-induced cytotoxicity and BDNF down-regulation in cultured rat hippocampal neurons.
Involvement of Akt/CREB signaling pathways in the protective effect of EPA against interleukin-1β-induced cytotoxicity and BDNF down-regulation in cultured rat hippocampal neurons.
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Akt/CREB 信号通路参与 EPA 对白细胞介素 1β 诱导的细胞毒性和培养的大鼠海马神经元 BDNF 下调的保护作用
DOI：
10.1186/s12868-018-0455-7
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发表时间：
2018-09-06
期刊：
影响因子：
2.4
通讯作者：
Wang Y
中科院分区：
文献类型：
--
作者：
Dong Y;Pu K;Duan W;Chen H;Chen L;Wang Y
我们已发表的资料表明，omega-3多不饱和脂肪酸二十碳五烯酸通过减轻白细胞介素1β(IL-1β)诱导的神经元损伤而发挥有益的作用，而上调脑源性神经营养因子的表达是其神经保护作用的重要组成部分。然而，EPA如何调控BDNF表达的机制仍不完全清楚。本研究探讨Akt/CREB信号通路在EPA影响BDNF表达及其神经保护作用中的作用。结果表明，IL-1EPA可降低海马神经元的存活率，且呈浓度依赖性，但β的神经保护作用可被AKT的抑制剂KRX-0401阻断。环丙沙星可改善IL-1β诱导的海马神经元Akt和CREB磷酸化水平的降低，以及IL-1β介导的脑源性神经营养因子的下调。然而，抑制Akt可逆转EPA对p-Akt、p-CREB和BDNF水平的影响。我们的数据表明，EPA对IL-1β诱导的细胞损伤和脑源性神经营养因子的减少具有神经保护作用，其作用可能是通过Akt/CREB信号通路实现的。
Our published data have indicated that the omega-3 polyunsaturated fatty acid eicosapentaenoic acid (EPA) provides beneficial effects by attenuating neuronal damage induced by interleukin-1β (IL-1β), and up-regulation of the expression of brain-derived neurotrophic factor (BDNF) represents a crucial part in the neuroprotective effect of EPA. However, the mechanisms of how EPA regulates BDNF expression remains incompletely understood. The present study investigated the role of Akt/CREB signaling in the effect of EPA on BDNF expression and its neuroprotective effect. The present results showed that IL-1β reduced hippocampal neuronal viability and that EPA showed a concentration-dependent neuroprotective effect, but the neuroprotective effects of EPA were abolished by inhibition of Akt using KRX-0401, an inhibitor of Akt. Treatment of hippocampal neurons with EPA also ameliorated the decrease in Akt and CREB phosphorylation induced by IL-1β and BDNF down-regulation mediated by IL-1β. However, inhibition of Akt reversed the effect of EPA on levels of p-Akt, p-CREB, and BDNF. Our data indicate that EPA elicited neuroprotection toward IL-1β-induced cell damage and BDNF decrease and that its effects potentially occurred via the Akt/CREB signaling pathway.
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影响因子：
9.3
作者：
Carlos AJ;Tong L;Prieto GA;Cotman CW
通讯作者：
Cotman CW
影响因子：
9.9
作者：
Benarroch, Eduardo E.
通讯作者：
Benarroch, Eduardo E.
DOI：
10.1016/0736-5748(94)00072-b
发表时间：
1995-06-01
影响因子：
1.8
作者：
ARAUJO, DM;COTMAN, CW
通讯作者：
COTMAN, CW
神经元活动通过成熟神经元中的 Polycomb 去抑制和 CREB/CBP/JMJD3 激活来控制 Bdnf 表达。
影响因子：
16.6
作者：
Palomer E;Carretero J;Benvegnù S;Dotti CG;Martin MG
通讯作者：
Martin MG
膳食二十碳五烯酸使海马 omega-3 和 6 多不饱和脂肪酸谱正常化，减弱神经胶质活化并调节中枢白细胞介素 1β 给药引起的神经炎症啮齿动物模型中的 BDNF 功能
影响因子：
5
作者：
Dong, Yilong;Xu, Min;Song, Cai
通讯作者：
Song, Cai