Protective effect of curcumin against chronic alcohol-induced cognitive deficits and neuroinflammation in the adult rat brain

Neuroscience. 2013 Aug 6;244:147-58. doi: 10.1016/j.neuroscience.2013.03.042. Epub 2013 Apr 9.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylcholinesterase / metabolism
  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
  • Behavior, Animal / drug effects
  • Caspase 3 / metabolism
  • Cerebral Cortex / drug effects*
  • Cerebral Cortex / metabolism
  • Cerebral Cortex / pathology
  • Cognition Disorders / chemically induced
  • Cognition Disorders / drug therapy*
  • Curcumin / pharmacology*
  • Curcumin / therapeutic use
  • Cytokines / metabolism
  • Dose-Response Relationship, Drug
  • Drug Evaluation, Preclinical
  • Ethanol / toxicity*
  • Hippocampus / drug effects*
  • Hippocampus / metabolism
  • Hippocampus / pathology
  • Inflammation / chemically induced
  • Inflammation / drug therapy*
  • Male
  • Neuroprotective Agents / pharmacology*
  • Neuroprotective Agents / therapeutic use
  • Nitrites / metabolism
  • Oxidative Stress / drug effects
  • Rats
  • Transcription Factor RelA / metabolism


  • Anti-Inflammatory Agents, Non-Steroidal
  • Cytokines
  • Neuroprotective Agents
  • Nitrites
  • Transcription Factor RelA
  • Ethanol
  • Acetylcholinesterase
  • Caspase 3
  • Curcumin