Formononetin attenuates Aβ25-35-induced cytotoxicity in HT22 cells via PI3K/Akt signaling and non-amyloidogenic cleavage of APP.

Abstract:

:Amyloid beta (Aβ) 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 Aβ25-35-induced neurotoxicity in HT22 cells. We found that Form significantly increased the viability of HT22 cells but decreased the cell apoptosis when challenging with Aβ25-35. The inhibitory effects of Form were associated with PI3K/Akt signaling pathway as PI3K inhibitor (LY294002) or ERα specific inhibitor (MPP) blocked the effects. Form also accelerated the non-amyloidogenic process of amyloid precursor protein (APP) by enhancing α-secretase activity and sAPPα release. Altogether, our findings may provide a novel therapeutic target to treat AD sufferers.

journal_name

Neurosci Lett

journal_title

Neuroscience letters

authors

Chen L,Ou S,Zhou L,Tang H,Xu J,Guo K

doi

10.1016/j.neulet.2016.12.064

subject

Has Abstract

pub_date

2017-02-03 00:00:00

pages

36-42

eissn

0304-3940

issn

1872-7972

pii

S0304-3940(16)31012-6

journal_volume

639

pub_type

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