Abstract
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 (10 mg/kg or 100 mg/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 α-smooth muscle actin ( α-SMA), desmin, and tissue inhibitor of metalloproteinase-1 (TIMP-1) protein in the liver. Nuclear factor κ B p65 (NF- κBp65) protein in nucleus and transforming growth factor β1 (TGF- β1) protein in cytoplasm were detected by Western blot. NF- κBp65, TGF- β1, 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- κBp65, TGF- β1 and TIMP-1 protein, and mRNA were significantly decreased in these animals. The expressions of α-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- κB signaling pathway to prevent the progression of liver cirrhosis.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
