Fucoxanthin, a Marine Carotenoid, Attenuates beta-Amyloid Oligomer-Induced Neurotoxicity Possibly via Regulating the PI3K/Akt and the ERK Pathways in SH-SY5Y Cells

TitleFucoxanthin, a Marine Carotenoid, Attenuates beta-Amyloid Oligomer-Induced Neurotoxicity Possibly via Regulating the PI3K/Akt and the ERK Pathways in SH-SY5Y Cells
Publication TypeJournal Article
Year of Publication2017
AuthorsLin JJ, Yu J., Zhao J.Y, Zhang K, Zheng J.C, Wang J.L, Huang C.H, Zhang J.R, Yan X.J, Gerwick WH, Wang Q.W, Cui W., He S.
JournalOxidative Medicine and Cellular Longevity
Date Published2017/08
Type of ArticleArticle
ISBN Number1942-0900
Accession NumberWOS:000407095100001
Keywordsactivation; alzheimers-disease; in-vitro; inflammation; inhibition; long-term potentiation; mechanisms; model; nf-kappa-b; oxidative; stress
Abstract

Alzheimer's disease (AD), the most common neurodegenerative disorder, is characterized by neurofibrillary tangles, synaptic impairments, and loss of neurons. Oligomers of beta-amyloid (A beta) are widely accepted as the main neurotoxins to induce oxidative stress and neuronal loss in AD. In this study, we discovered that fucoxanthin, a marine carotenoid with antioxidative stress properties, concentration dependently prevented A beta oligomer-induced increase of neuronal apoptosis and intracellular reactive oxygen species in SH-SY5Y cells. A beta oligomers inhibited the prosurvival phosphoinositide 3-kinase (PI3K)/Akt cascade and activated the proapoptotic extracellular signal-regulated kinase (ERK) pathway. Moreover, inhibitors of glycogen synthase kinase 3 beta (GSK3 beta) and mitogen-activated protein kinase (MEK) synergistically prevented A beta oligomer-induced neuronal death, suggesting that the PI3K/Akt and ERK pathways might be involved in A beta oligomer-induced neurotoxicity. Pretreatment with fucoxanthin significantly prevented A beta oligomer-induced alteration of the PI3K/Akt and ERK pathways. Furthermore, LY294002 and wortmannin, two PI3K inhibitors, abolished the neuroprotective effects of fucoxanthin against A beta oligomer-induced neurotoxicity. These results suggested that fucoxanthin might prevent A beta oligomer-induced neuronal loss and oxidative stress via the activation of the PI3K/Akt cascade as well as inhibition of the ERK pathway, indicating that further studies of fucoxanthin and related compounds might lead to a useful treatment of AD.

DOI10.1155/2017/6792543
Student Publication: 
No
Research Topics: 
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