Role of curcumin on changes of PPAR-gamma expression, NF-kappa B activation and oxidative stress in rats with alcoholic hepatitis

Abstract

Alcohol oxidation generates toxic metabolites and induces oxidative stress which contributes to the pathogenesis of alcoholic liver disease. Curcumin, the active ingredient of Curcuma longa Linn., is a potent antioxidant and anti-inflammation. The present study determined the possible mechanism that curcumin could attenuate liver injury induced by alcohol in rats. Female Sprague-Dawley rats were divided into four groups. Control group was fed distilled water. Alcohol group was fed 50% alcohol (7.5 g/kg BW day). Treatment groups were fed curcumin dissolved in 50% alcohol (7.5 g/kg BW day) at a dose of 400 mg/kg BW a day and 1,200 mg/kg BW a day, respectively. Alcohol or curcumin was treated via an intragastric tube for 4 weeks. Rats were sacrificed and liver samples were collected at the end of the study. The liver histopathology in alcohol group revealed mild to moderate steatosis, and mild necroinflammation. Level of hepatic malondialdehyde (MDA), hepatocyte apoptosis and NF-B activation increased significantly when compared with control group. Curcumin treatments resulted in improving liver pathology, decreasing the elevation of hepatic MDA and inhibiting NF-B activation. The 400 mg/kg BW of curcumin treatment revealed only a trend of decreased hepatocyte apoptosis. However, the results of superoxide dismutase activity and PPAR protein expression showed no difference among the groups. In conclusion, curcumin could attenuate liver injury induced by alcohol through the reduction of oxidative stress and inhibition of NF-B activation. In addition, curcumin might have a trend to decrease hepatocyte apoptosis. PPAR protein expression may not change in early stage of alcohol-induced liver injury.