Protective effects of the resveratrol analog piceid in dopaminergic SH-SY5Y cells
Document Type
Article
Publication Date
2-1-2018
Publication Title
Archives of Toxicology
Keywords
Antioxidant, Apoptosis, Bcl-2, Dopamine, ERK1/2, ERK5, Oxidative stress, Phytochemicals, Piceid, Polydatin, Resveratrol, SH-SY5Y, Toxicity caspase
ISSN
0340-5761
Volume
92
Issue/No.
2
First Page
669
Last Page
677
Abstract
Age-related motor deficits, such as loss of balance and coordination, are caused, in part, by loss of dopaminergic neurons. Oxidative stress is known to play a role in this neuronal loss. Resveratrol, a natural antioxidant with anticancer and anti-inflammatory potential, has been shown to protect dopaminergic-like cells (SH-SY5Y) against oxidative stress. However, the low bioavailability of resveratrol makes it worthwhile to explore newer compounds with similar properties. Piceid (RV8), an analog of resveratrol, has greater bioavailability than resveratrol, and our studies found that piceid (10, 20, 30 µM) protects SH-SY5Y cells against oxidative stress. Our investigations also found that the neuroprotection afforded by piceid was decreased when the MAP kinases, ERK1/2 and ERK5, were independently inhibited. Since oxidative stress is considered a master operator of apoptosis, our study also scrutinized dopamine-induced apoptosis and whether caspase-3/7 and Bcl-2 are involved, following piceid pretreatment followed by dopamine exposure. Our findings suggested that piceid pretreatment inhibited the dopamine-induced increase in caspase-3/7 activity and dopamine-induced loss of Bcl-2 expression. Overall, these findings suggest that the neuroprotective effects of piceid are mediated via the activation of ERK1/2, ERK5, and inhibition of apoptosis caused by oxidative stress.
NSUWorks Citation
Potdar, Sneha; Parmar, Mayur S.; Ray, Sidhartha D.; and Cavanaugh, Jane E., "Protective effects of the resveratrol analog piceid in dopaminergic SH-SY5Y cells" (2018). HPD Articles. 19.
https://nsuworks.nova.edu/hpd_facarticles/19
ORCID ID
0000-0003-4970-9857
DOI
10.1007/s00204-017-2073-z
Copyright
© Springer-Verlag GmbH Germany 2017