Abstract
BackgroundOur 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.ResultsThe 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.ConclusionsOur 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.
Highlights
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
The present results showed that IL-1β caused neurotoxicity in hippocampal neurons, and EPA attenuated cell damage and BDNF down-regulation in correlation with
This notion is supported by the following observations: (1) Treatment with IL-1β in cultured hippocampal neurons caused cell damage, while EPA significantly reversed the toxic effect of IL-1β; (2) Akt and cAMP-response element binding protein (CREB) phosphorylation was inhibited by IL-1β, while EPA prevented this inhibition; (3) inhibition of Akt/CREB blocked the neuroprotective effect of EPA toward IL-1β-induced cell damage; (4) the beneficial effect of EPA on BDNF expression was blocked by inhibiting Akt/CREB signaling
Summary
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. 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. Eicosapentaenoic acid (EPA) is an omega-3 polyunsaturated fatty acid that cannot be synthesized by the human body. We have reported that EPA markedly attenuated the IL-1β-induced BDNF decrease in the hippocampus, which may provide beneficial effects against inflammation-associated neurodegenerative changes [13]. The mechanisms underlying how EPA modulates BDNF still remain unclear
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