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Journal of Biomedicine and Biotechnology
Volume 2009, Article ID 981963, 8 pages
Research Article

Curcumin Decreased Oxidative Stress, Inhibited NF- B Activation, and Improved Liver Pathology in Ethanol-Induced Liver Injury in Rats

1Department of Physiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
2Department of Dietatic, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
3Department of Pathology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand

Received 23 February 2009; Accepted 1 May 2009

Academic Editor: Stelvio M. Bandiera

Copyright © 2009 Suchittra Samuhasaneeto et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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- B 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- B activation. The 400 mg/kg bw of curcumin treatment revealed only a trend of decreased hepatocyte apoptosis. However, the results of SOD activity, PPAR 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- B activation.