The evaluation of sodium molybdate effect on liver fibrosis in a rat model of bile duct ligation

The accumulation of hydrophobic bile acids in bile duct ligation (BDL) animal model¡ plays a pivotal role in the induction of hepatic fibrosis. Cholestatic liver fibrosis¡ characterized by excessive accumulation of extracellular matrix (ECM) proteins¡ is associated with bile acidinduced oxidative stress and lipid peroxidation. Molybdenum is an essential trace element which acts as a cofactor in many detoxification system enzymes. The results of our previous study suggested that sodium molybdate could be used as a hepatoprotective agent against toxicity caused by carbon tetrachloride in rats .The aim of the present study was to evaluate the therapeutic or the anti-hepatofibrotic effects of sodium molybdate in a bile duct ligation (BDL)- induced cholestatic fibrosis model in rats .After BDL¡ rats were given sodium molybdate (0.05 or 0.1 or 0.2 g/kg) or urosodeoxycholic acid (UDCA¡ 25 mg/kg) orally for 45 consecutive days (once per day). BDL markedly induced the accumulation of collagen¡ as well as infiltration of inflammatory cells¡ hepatocyte necrosis and bile duct hyperplasia¡ as determined by Masson’s trichrome staining. These alterations were significantly attenuated by sodium molybsdate administration (0.1 and 0.2 g/kg). Simultaneously treatment of sodium molybdate may inhibit the liver fibrosis in a BDL model of cholestatic rats. Our data suggest that sodium molybdate may exert its antifibrotic effects via inhibition of ECM proteins.