title: Protective effect of curcumin against chronic alcohol-induced cognitive deficits and neuroinflammation in the adult rat brain.
abstract: 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-1 beta (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.
authors.affiliation: Pharmacology Research Laboratory, University Institute of Pharmaceutical Sciences, UGC Center of Advanced Study, Panjab University, Chandigarh 160 014, India.
authors.forename: V
authors.initials: V
authors.lastname: Tiwari
authors.forename: K
authors.initials: K
authors.lastname: Chopra
mesh_terms: D000110:Acetylcholinesterase / Q000378:metabolism; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology / Q000627:therapeutic use; D001522:Behavior, Animal / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism; D002540:Cerebral Cortex / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D003072:Cognition Disorders / Q000139:chemically induced / Q000188:drug therapy*; D003474:Curcumin / Q000494:pharmacology* / Q000627:therapeutic use; D016207:Cytokines / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004353:Drug Evaluation, Preclinical; D000431:Ethanol / Q000633:toxicity*; D006624:Hippocampus / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D007249:Inflammation / Q000139:chemically induced / Q000188:drug therapy*; D008297:Male; D018696:Neuroprotective Agents / Q000494:pharmacology* / Q000627:therapeutic use; D009573:Nitrites / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D051996:Transcription Factor RelA / Q000378:metabolism
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D016207:Cytokines; D018696:Neuroprotective Agents; D009573:Nitrites; D051996:Transcription Factor RelA; D000431:Ethanol; D000110:Acetylcholinesterase; D053148:Caspase 3; D003474:Curcumin