AIM: To evaluate the effect of rosiglitazone in a murine model of liver fibrosis induced by Schistosoma japonicum infection.METHODS: A total of 50 mice were randomly and averagely divided into groups A, B, C, D and E. The mice in group A served as normal controls, while those in the other four groups were infected with Schistosoma japonicum to induce the model of liver fibrosis. Besides, the mice in groups C, D and E were treated with praziquantel, rosiglitazone and praziquantel plus rosiglitazone, respectively. NF-κB binding activity and expression of PPARγ-mRNA were determined by Western blot assay and real-time quantitative PCR.Radioimmunonassay technique was used to detect the serum content changes of TNF-α and IL-6. Histological specimens were stained with HE. Expression of TGF-β1,a-smooth muscle actin and type Ⅰ and type Ⅲ collagen was detected by immunohistochemistry and multimedia color pathographic analysis system.RESULTS: Inflammation and fibrosis in the rosiglitazone plus praziquantel treatment group (group E) were lightest among the mice infected with Schistosoma (P < 0.05).To further explore the mechanism of rosiglitazone action,we found that rosiglitazone can significantly increase the expression of PPARγ, [E: -18.212 ± (-3.909) vs B:-27.315 ± (-6.348) and C: -25.647 ± (-5.694), P < 0.05],reduce the NF-κB binding activity (E: 88.89 ± 19.34 vs B: 141.11 ± 15.37, C: 112.89 ± 20.17 and D: 108.89 ±20.47, P < 0.05), and lower the serum level of TNF-α (E:1.613 ± 0.420 ng/mL vs B: 2.892 ± 0.587 ng/mL, C: 2.346± 0.371 ng/mL and D: 2.160 ± 0.395 ng/mL, P < 0.05)and IL-6 (E: 0.106 ± 0.021 ng/mL vs B: 0.140 ± 0.031ng/mL and C: 0.137 ± 0.027 ng/mL, P < 0.05) in mice with liver fibrosis. Rosiglitazone can also substantially reduce the hepatic expression of TGF-β1,α-SMA type Ⅰ and type Ⅲ collagen in mice with liver fibrosis.CONCLUSION: The activation of PPARγ by its ligand can retard liver fibrosis and suggest the use of rosiglitazone for the treatment of liver fibrosis due to Schistosoma japonicum infection.