Scallop-derived plasmalogen attenuates amyloid beta-induced inflammation and apoptosis in SH-SY5Y cells

Abstract

BackgroundsWith an increase in the world's aging population, candidate substances for the management of neurodegenerative diseases, including Alzheimer's disease (AD), have received considerable attention. Amyloid beta (A beta) peptide, the leading cause of AD, induces synaptic deficits, eventually leading to cognitive impairment. Plasmalogen is a subclass of glycerophospholipids containing a vinyl ether group in the glycerol backbone which has various efficacies.ObjectivesIn this study, we investigated the mechanisms of scallop-derived plasmalogen (SPL) in neurotoxicity in human neurons, which remain incompletely understood. SH-SY5Y human neuroblastaoma cells were treated with A beta 1-42, a major component of amyloid deposits in AD brains.ResultsSPL inhibited the phosphorylation of glycogen synthase kinase 3 beta and tau induced by A beta. In addition, SPL decreased A beta generation by downregulating the expression of amyloid precursor protein (APP) and beta-site APP cleaving enzyme 1. Furthermore, SPL suppressed the release of pro-inflammatory cytokines and expression of apoptotic proteins induced by A beta.ConclusionOur study indicates that SPL would reduce A beta-induced neurotoxicity associated with inflammation and apoptosis in human neuroblastoma cells.