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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

BACKGROUND: 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) represen...

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Detalles Bibliográficos
Autores principales: Dong, YiLong, Pu, KangJing, Duan, WenJing, Chen, HuiCheng, Chen, LiXing, Wang, YanMei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6128001/
https://www.ncbi.nlm.nih.gov/pubmed/30189852
http://dx.doi.org/10.1186/s12868-018-0455-7
Descripción
Sumario:BACKGROUND: 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. RESULTS: 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. CONCLUSIONS: 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.