Resveratrol and pinostilbene confer neuroprotection against aging-related deficits through an ERK1/2-dependent mechanism

Age-related declines in motor function may be due, in part, to an increase in oxidative stress in the aging brain leading to dopamine (DA) neuronal cell death. In this study, we examined the neuroprotective effects of natural antioxidants resveratrol and pinostilbene against age-related DAergic cell...

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Bibliographic Details
Published in:The Journal of nutritional biochemistry 2018-04, Vol.54, p.77-86
Main Authors: Allen, Erika N., Potdar, Sneha, Tapias, Victor, Parmar, Mayur, Mizuno, Cassia S., Rimando, Agnes, Cavanaugh, Jane E.
Format: Article
Language:English
Subjects:
Aging
antioxidants
brain
cell death
cell viability
dietary supplements
dopamine
ERK1/2
males
metabolites
mice
neurons
neuroprotective effect
oxidative stress
Pinostilbene
Resveratrol
senescence (aging)
SH-SY5Y
Striatum
Substantia nigra
transporters
tyrosine 3-monooxygenase
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Summary:Age-related declines in motor function may be due, in part, to an increase in oxidative stress in the aging brain leading to dopamine (DA) neuronal cell death. In this study, we examined the neuroprotective effects of natural antioxidants resveratrol and pinostilbene against age-related DAergic cell death and motor dysfunction using SH-SY5Y neuroblastoma cells and young, middle-aged, and old male C57BL/6 mice. Resveratrol and pinostilbene protected SH-SY5Y cells from a DA-induced decrease in cell viability. Dietary supplementation with resveratrol and pinostilbene inhibited the decline of motor function observed with age. While DA and its metabolites (DOPAC and HVA), dopamine transporter, and tyrosine hydroxylase levels remain unchanged during aging or treatment, resveratrol and pinostilbene increased ERK1/2 activation in vitro and in vivo in an age-dependent manner. Inhibition of ERK1/2 in SH-SY5Y cells decreased the protective effects of both compounds. These data suggest that resveratrol and pinostilbene alleviate age-related motor decline via the promotion of DA neuronal survival and activation of the ERK1/2 pathways.
ISSN:0955-2863
1873-4847
DOI:10.1016/j.jnutbio.2017.10.015