Protective effect of a sesamin derivative, 3-bis (3-methoxybenzyl) butane-1, 4-diol on Ab-stressed PC12 cells

Amyloid beta-protein (Ab) is involved in thepathogenesis of Alzheimer’s disease (AD). Ab induces freeradical production in neuronal cells, leading to oxidativestress and up-regulation of c-Jun N-terminal kinases (JNK),extracellular-signal-regulated kinases (ERK), p38 mitogenactivatedprotein kinase (MAPK) pathways and pro-apoptoticBax expression. Sesamin has been shown to haveprotection to several models of neurodegenerative diseasesby its antioxidant and anti-inflammatory properties. In thepresent study, we examined the neuroprotective effect of asesamin derivative, 3-bis (3-methoxybenzyl) butane-1,4-diol (BBD) on Ab1–42 induced cytotoxicity of PC12 cells. Ab1–42 induced lipid peroxidation, calcium, reactive oxygenspecies from the PC12 cells. The effect of BBD onthese harmful factors and the related signaling pathwayswere examined by biochemical and western blot assays. The result showed that BBD protected PC12 cells fromAb1–42 induced cytotoxicity with the increased cell viabilityand acetylcholine release, and the decreased lactatedehydrogenase, malondialdehyde and calcium release. BBD significantly reduced Ab-induced JNK, ERK, p38MAPK pathways and Bax expression in PC12 cells. Therefore the neuroprotective effect of BBD on Abinducedcytotoxicity was involved with antioxidant andanti-inflammatory effects. The result would help thedevelopment of new CNS drug for protection of AD.