Curcumin decreased oxidative stress, inhibited NF-kappaB activation, and improved liver pathology in ethanol-induced liver injury in rats

J Biomed Biotechnol. 2009:2009:981963. doi: 10.1155/2009/981963. Epub 2009 Jul 6.

Abstract

To study the mechanism of curcumin-attenuated inflammation and liver pathology in early stage of alcoholic liver disease, female Sprague-Dawley rats were divided into four groups and treated with ethanol or curcumin via an intragastric tube for 4 weeks. A control group treated with distilled water, and an ethanol group was treated with ethanol (7.5 g/kg bw). Treatment groups were fed with ethanol supplemented with curcumin (400 or 1 200 mg/kg bw). The liver histopathology in ethanol group revealed mild-to-moderate steatosis and mild necroinflammation. Hepatic MDA, hepatocyte apoptosis, and NF-kappaB activation increased significantly in ethanol-treated group when compared with control. Curcumin treatments resulted in improving of liver pathology, decreasing the elevation of hepatic MDA, and inhibition of NF-kappaB activation. The 400 mg/kg bw of curcumin treatment revealed only a trend of decreased hepatocyte apoptosis. However, the results of SOD activity, PPARgamma protein expression showed no difference among the groups. In conclusion, curcumin improved liver histopathology in early stage of ethanol-induced liver injury by reduction of oxidative stress and inhibition of NF-kappaB activation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Apoptosis / drug effects
  • Curcumin / pharmacology*
  • Ethanol
  • Fatty Liver, Alcoholic / metabolism
  • Fatty Liver, Alcoholic / pathology
  • Female
  • Histocytochemistry
  • Inflammation / metabolism
  • Liver Diseases, Alcoholic / drug therapy*
  • Liver Diseases, Alcoholic / metabolism*
  • Liver Diseases, Alcoholic / pathology
  • Malondialdehyde / metabolism
  • Necrosis / metabolism
  • Oxidative Stress / drug effects*
  • PPAR gamma / biosynthesis
  • Rats
  • Rats, Sprague-Dawley
  • Superoxide Dismutase / metabolism
  • Transcription Factor RelA / antagonists & inhibitors*
  • Transcription Factor RelA / biosynthesis

Substances

  • PPAR gamma
  • Transcription Factor RelA
  • Ethanol
  • Malondialdehyde
  • Superoxide Dismutase
  • Curcumin