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
Abstract
Background: Our printed data have established that the omega-3 polyunsaturated essential fatty acid eicosapentaenoic acidity (Environmental protection agency) provides advantageous effects by attenuating neuronal damage caused by interleukin-1ß (IL-1ß), or more-regulating the expression of brain-derived neurotrophic factor (BDNF) represents an essential part within the neuroprotective aftereffect of Environmental protection agency. However, the mechanisms of methods Environmental protection agency regulates BDNF expression remains incompletely understood. The current study investigated the function of Akt/CREB signaling within the aftereffect of Environmental protection agency on BDNF expression and it is neuroprotective effect.
Results: The current results demonstrated that IL-1ß reduced hippocampal neuronal viability which Environmental protection agency demonstrated a concentration-dependent neuroprotective effect, however the neuroprotective results of Environmental protection agency were abolished by inhibition of Akt using KRX-0401, an inhibitor of Akt. Management of hippocampal neurons with Environmental protection agency also ameliorated the reduction in Akt and CREB phosphorylation caused by IL-1ß and BDNF lower-regulation mediated by IL-1ß. However, inhibition of Akt reversed the result of Environmental protection agency on amounts of p-Akt, p-CREB, and BDNF.
Conclusions: Our data indicate that Environmental protection agency elicited KRX-0401 neuroprotection toward IL-1ß-caused cell damage and BDNF decrease which its effects potentially happened through the Akt/CREB signaling path.