Thalidomide salvages lethal hepatic necroinflammation and accelerates recovery from cirrhosis in rats

Background/Aims The authors investigated the feasibility of thalidomide employed to treat liver fibrosis. Methods A cirrhotic model was established using Sprague–Dawley rats fed thioacetamide. Thalidomide-treated group was given thalidomide (10 mg/kg/day) intraperitoneally for 10 consecutive days. Mortality, histopathological changes, TNFα, TGFβ1, TIMP-1 and TIMP-2 were determined. Expression of TNFα and TGFβ1 mRNA of Kupfferʹs cells derived from the experimental rats were determined. Results The mortality rates of thalidomide-treated group and vehicle-treated group were 8 and 32%, respectively. The total Knodell score of thalidomide-treated rats was lower than those of vehicle-treated rats. Micro-nodular cirrhosis resolved grossly in thalidomide-treated rats on day 28; while vehicle-treated rats continued to display uneven liver surface on day 28. Expression of TNFα, TGFβ1, TIMP-1, and TIMP-2 was decreased in thalidomide-treated rats compared to those treated with vehicles. Finally, the expression of TNFα and TGFβ1 mRNA of Kupfferʹs cells derived from rats treated with thalidomide were much lower than those treated with vehicle. Conclusions Thalidomide salvages lethal hepatic necroinflammation, accelerates recovery from cirrhosis in rats, and works by suppressing of TNFα and TGFβ1 production of Kupfferʹs cells.