AIM: To observe the anti-liver fibrosis effect of Astragalus complanatus flavonoids(ACF) in rats. METHODS: The liver fibrosis model in rats was established by injecting interperitoneally 0.2 mL/100 g 0.5% dimethylnitrosamine, thrice a week. Meanwhile, the rats were administered ACF(30, 60, 120 mg/kg) or colchicine(0.1 mg/kg) once a day for 1 mo. Serum N-propeptide of type Ⅰ procollagen(PINP) and type Ⅲ procollagen(PIIINP) was measured using ELISA. Malondialdehyde(MDA) and superoxide dismutase(SOD) in hepatic tissue were evaluated. Matrix metal protease-1(MMP-1) mRNA expression was assayed by RT-PCR and the protein expression of tissue inhibitor of metal protease-1(TTMP-1) was analyzed by immunohistochemistry. RESULTS: In the ACF groups, SOD activity increased and MDA content decreased in comparison to the liver fibrosis model group. The serum PINP and PIIINP contents in ACF-2 and -3 group decreased compared to those in model group. In ACF-2 and -3 group, the expression of MMP-1 mRNA increased significantly and the protein expression of TTMP-1 decreased compared to that in model group. CONCLUSION: The antifibrotic mechanisms of ACF are associated with its influence on lipid peroxidation and collagen synthesis and degradation. AIM: To observe the anti-liver fibrosis effect of Astragalus complanatus flavonoids (ACF) in rats. METHODS: The liver fibrosis model in rats was established by injecting interperitoneally 0.2 mL/100 g 0.5% dimethylnitrosamine, thrice a week. at the same time, the rats Were administered ACF(30, 60, 120 mg/kg) or colchicine(0.1 mg/kg) once a day for 1 mo. Serum N-propeptide of type I procollagen(PINP) and type III procollagen(PIIINP) was measured using ELISA Malondialdehyde (MDA) and superoxide dismutase (SOD) in hepatic tissue were evaluated. Matrix metal protease-1 (MMP-1) mRNA expression was assayed by RT-PCR and the protein expression of tissue inhibitor of metal protease-1 (TTMP- 1) was analyzed by immunohistochemistry. RESULTS: In the ACF groups, SOD activity increased and MDA content decreased in comparison to the liver fibrosis model group. The serum PINP and PIIINP contents in ACF-2 and -3 group decreased to to those in model Group. In ACF-2 and -3 group, the expression of MMP-1 mRN Conclusions: The antifibrotic mechanisms of ACF are associated with its influence on lipid peroxidation and collagen synthesis and degradation.