Article ID Journal Published Year Pages File Type
4337931 Neuroscience 2013 12 Pages PDF
Abstract

•Ethanol-exposed rats showed impaired spatial navigation in both Morris water maze test and elevated plus maze task.•Memory impairment was coupled with enhanced oxidative–nitrosative stress and inflammatory signaling.•Co-administration with curcumin significantly prevented all the behavioral, biochemical and molecular deficits.

Chronic alcohol intake is known to induce the selective neuronal damage associated with increase oxidative–nitrosative stress and activation of inflammatory cascade finally resulting in cognitive deficits. In the present study, we investigated the protective effect of curcumin, a potent natural anti-oxidant and anti-inflammatory molecule against chronic alcohol-induced cognitive dysfunction and nuclear factor kappa beta (NF-κβ) mediated inflammatory signaling in the brain of rats chronically administered ethanol. Male Wistar rats were given ethanol (10 g/kg; oral gavage) for 10 weeks, and treated with curcumin (15, 30 and 60 mg/kg) for the same duration. Ethanol-exposed rats showed impaired spatial navigation in the Morris water maze test and poor retention in the elevated plus maze task which was coupled with enhanced acetylcholinesterase activity, increased oxidative–nitrosative stress, cytokines (tumor necrosis factor alpha (TNF-α) and interleukin-1beta (IL-1β)), NF-kβ and caspase-3 levels in different brain regions (cerebral cortex and hippocampus) of ethanol-treated rats. Co-administration with curcumin significantly and dose-dependently prevented all the behavioral, biochemical and molecular alterations in rats chronically administered ethanol. Thus, findings from the current study demonstrates the possible involvement of oxidative–nitrosative stress mediated cytokine release and inflammatory signaling in chronic alcohol-induced cognitive dysfunction and also suggests the effectiveness of curcumin in preventing cognitive deficits associated with chronic alcohol consumption.

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