Formononetin attenuates A beta(25-35)-induced cytotoxicity in HT22 cells via PI3K/Akt signaling and non-amyloidogenic cleavage of APP

摘要

Amyloid beta (A beta) is the main component of the amyloid plaques that accumulate in the brains of Alzheimer patients. Here, we reported the protective role of Formononetin (Form) against A beta(25-35)-induced neurotoxicity in HT22 cells. We found that Form significantly increased the viability of HT22 cells but decreased the cell apoptosis when challenging with A beta(25-35). The inhibitory effects of Form were associated with PI3K/Akt signaling pathway as PI3K inhibitor (LY294002) or ER alpha specific inhibitor (MPP) blocked the effects. Form also accelerated the non-amyloidogenic process of amyloid precursor protein (APP) by enhancing alpha-secretase activity and sAPP alpha release. Altogether, our findings may provide a novel therapeutic target to treat AD sufferers. (C) 2016 Elsevier Ireland Ltd. All rights reserved.