Allopurinol reverses liver damage induced by chronic carbon tetrachloride treatment by decreasing oxidative stress, TGF-β production and NF-κB nuclear translocation.

Allopurinol is an inhibitor of xanthine oxidase. The aim of this work was to evaluate the efficacy of allopurinol to reverse the experimental cirrhosis induced by CCl4. Rats received CCl4 for 8 weeks, and immediately after allopurinol was administered for 4 weeks more. Allopurinol reversed all markers of liver damage and oxidative stress to normal values, restoring the metabolic capacity of the liver. Chronic injury by CCl4 induced significant overexpression of profibrogenic cytokine TGF-β, while allopurinol decreased this production and consequently decreased the collagen content. Moreover, allopurinol is capable of partially inhibiting NF-κB. These findings suggest that allopurinol is capable of reversing the cirrhosis induced by CCl4, modulating oxidative stress, TGF-β expression and NF-κB nuclear translocation.