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

Subject Areas : Journal of Comparative Pathobiology

مهسا Ale Ebrahim, ¹ , اکرم Eidi, . ² , P. Mortazavi, ³ , S.M Tavangar, ⁴ , داریوش Minai Tehrani, ⁵

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Received: 2014-01-20 Accepted : 2014-04-29 Published : 2015-01-21

Keywords: Bile duct ligation (BDL), Cholestasis, Liver fibrosis, Rat, Sodium molybdate,

Abstract :

The accumulation of hydrophobic bile acids in bile duct ligation (BDL) animal model, plays apivotal role in the induction of hepatic fibrosis. Cholestatic liver fibrosis, characterized byexcessive accumulation of extracellular matrix (ECM) proteins, is associated with bile acidinducedoxidative stress and lipid peroxidation. Molybdenum is an essential trace element whichacts as a cofactor in many detoxification system enzymes. The results of our previous studysuggested that sodium molybdate could be used as a hepatoprotective agent against toxicitycaused by carbon tetrachloride in rats .The aim of the present study was to evaluate thetherapeutic 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 (0.05or 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 ofinflammatory cells, hepatocyte necrosis and bile duct hyperplasia, as determined by Masson’strichrome staining. These alterations were significantly attenuated by sodium molybsdateadministration (0.1 and 0.2 g/kg). Simultaneously treatment of sodium molybdate may inhibitthe liver fibrosis in a BDL model of cholestatic rats. Our data suggest that sodium molybdatemay exert its antifibrotic effects via inhibition of ECM proteins.