Thalidomide prevents rat liver cirrhosis via inhibition of oxidative stress.

This study investigated the effect of thalidomide on oxidative stress in rat liver cirrhosis. The cirrhosis of rat was induced by intraperitoneal injection of carbon tetrachloride thrice weekly; meanwhile, thalidomide (10mg/kg or 100mg/kg) was given daily by intragastric administration for 8 weeks. The content of oxidative stress parameters, including superoxide dismutase, glutathione peroxidase, and malondialdehyde, in the liver was detected by biochemical assay. Immunohistochemistry revealed alpha-smooth muscle actin (alpha-SMA), desmin, and tissue inhibitor of metalloproteinase-1 (TIMP-1) protein in the liver. Nuclear factor kappa B p65 (NF-kappaBp65) protein in nucleus and transforming growth factor beta1 (TGF-beta1) protein in cytoplasm were detected by Western blot. NF-kappaBp65, TGF-beta1, and TIMP-1 mRNA levels in the liver were studied using reverse transcriptase polymerase chain reaction. Liver histopathology was significantly improved in rats given high doses of thalidomide. The content of oxidative stress parameters and the expressions of NF-kappaBp65, TGF-beta1 and TIMP-1 protein, and mRNA were significantly decreased in these animals. The expressions of alpha-SMA and Desmin protein were also significantly decreased in them. Thalidomide might exert an effect on the inhibition of oxidative stress via downregulation of NF-kappaB signaling pathway to prevent the progression of liver cirrhosis.