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It is important to identify agents that provide neuroprotection against ethanol neurotoxicity. Multiple mechanisms have been proposed for ethanol\u2010induced neurodegeneration, and oxidative stress is one of the most important mechanisms. Recent evidence indicates that glycogen synthase kinase 3\u03b2 (GSK3\u03b2) is a potential mediator of ethanol\u2010mediated neuronal death. Cyanidin\u20103\u2010glucoside (C3G), a member of the anthocyanin family, is a potent natural antioxidant. Our previous study suggested that C3G inhibited GSK3\u03b2 activity in neurons. Using a third trimester equivalent mouse model of ethanol exposure, we tested the hypothesis that C3G can ameliorate ethanol\u2010induced neuronal death in the developing brain. Intraperitoneal injection of C3G reduced ethanol\u2010meditated caspase\u20103 activation, neurodegeneration, and microglial activation in the cerebral cortex of 7\u2010day\u2010old mice. C3G blocked ethanol\u2010mediated GSK3\u03b2 activation by inducing phosphorylation at serine 9 while reducing the phosphorylation at tyrosine 216. C3G also inhibited ethanol\u2010stimulated expression of malondialdehyde (MDA) and p47phox, indicating that C3G alleviated ethanol\u2010induced oxidative stress. These results provide important insight into the therapeutic potential of C3G. \u00a9 2011 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.22689","type":"journal-article","created":{"date-parts":[[2011,6,10]],"date-time":"2011-06-10T17:29:49Z","timestamp":1307726989000},"page":"1676-1684","source":"Crossref","is-referenced-by-count":55,"title":["Cyanidin\u20103\u2010glucoside ameliorates ethanol neurotoxicity in the developing 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