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Cyanidin-3-glucoside reverses ethanol-induced inhibition of neurite outgrowth: role of glycogen synthase kinase 3 beta.

Authors
Chen-G; Bower-KA; Xu-M; Ding-M; Shi-XL; Ke-ZJ; Luo-J
Source
Neurotox Res 2009 May; 15(4):321-331
NIOSHTIC No.
20035324
Abstract
Ethanol is a potent teratogen for the developing central nervous system (CNS), and fetal alcohol syndrome (FAS) is the most common nonhereditary cause of mental retardation. Ethanol disrupts neuronal differentiation and maturation. It is important to identify agents that provide neuroprotection against ethanol neurotoxicity. Using an in vitro neuronal model, mouse Neuro2a (N2a) neuroblastoma cells, we demonstrated that ethanol inhibited neurite outgrowth and the expression of neurofilament (NF) proteins. Glycogen synthase kinase 3 beta (GSK3 beta), a multifunctional serine/threonine kinase negatively regulated neurite outgrowth of N2a cells; inhibiting GSK3 beta activity by retinoic acid (RA) and lithium induced neurite outgrowth, while over-expression of a constitutively active S9A GSK3 beta mutant prevented neurite outgrowth. Ethanol inhibited neurite outgrowth by activating GSK3 beta through the dephosphorylation of GSK3 beta at serine 9. Cyanidin-3-glucoside (C3G), a member of the anthocyanin family rich in many edible berries and other pigmented fruits, enhanced neurite outgrowth by promoting p-GSK3 beta(Ser9). More importantly, C3G reversed ethanol-mediated activation of GSK3 beta and inhibition of neurite outgrowth as well as the expression of NF proteins. C3G also blocked ethanol-induced intracellular accumulation of reactive oxygen species (ROS). However, the antioxidant effect of C3G appeared minimally involved in its protection. Our study provides a potential avenue for preventing or ameliorating ethanol-induced damage to the developing CNS.
Keywords
Central-nervous-system; Chemical-hypersensitivity; Chemical-reactions; Cell-biology; Cell-metabolism; Cellular-reactions; Laboratory-animals; Mental-disorders; Mental-illness; Neurotoxic-effects; Author Keywords: Alcohol; Development; Differentiation; Fetal alcohol syndrome; Neuroprotection
Contact
Jia Luo, University of Kentucky, Department of Internal Medicine, College of Medicine, 124C Combs Res Bldg,800 Rose St, Lexington, KY 40536
CODEN
NURRFI
Publication Date
20090501
Document Type
Journal Article
Email Address
jialuo888@uky.edu
Fiscal Year
2009
NTIS Accession No.
NTIS Price
Issue of Publication
4
ISSN
1029-8428
NIOSH Division
HELD
Source Name
Neurotoxicity Research
State
WV
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