OBJECTIVE： To investigate the effects of polydatin on protein expression of MMP-9 and TIMP-1 in renal tissue of renal fibrosis model rats， and to investigate the mechanism of delaying renal fibrosis in rats. METHODS： A total of 40 rats were randomly divided into sham operation group （normal saline）， model group （normal saline）， polydatin group （100 mg/kg） and benazepril group （positive control， 5 mg/kg）. Except for sham operation group， renal fibrosis rat model was induced by unilateral ureteral obstruction in other groups. 1 h after surgery， each group was given relevant medicine intragastrically， once a day. After 4 weeks of consecutive treatment， the contents of β2-microglobulin （β2-MG） and N-acetyl-β-D-glucosaminidase （NAG） in urine， serum contents of BUN and Cr were detected in each group. HE staining was used to observe and score pathological changes of renal tissue in rats. Protein expressions of MMP-9 and TIMP-1 in renal tissue of rats were determined by immunohistochemistry. RESULTS： Compared with sham operation group， the contents of β2-MG and NAG in urine， serum contents of BUN and Cr were increased significantly in model group （P＜0.05）， and pathological score and protein expressions of MMP-9 and TIMP-1 were also increased significantly （P＜0.01）. Compared with model group， protein expression of MMP-9 in renal tissue were increased continuously in polydatin group and benazepril group （P＜0.01）； other indexes were decreased significantly （P＜0.05 or P＜0.01）， and there was no statistical significance in each index between polydatin group and benazepril group （P＞0.05）. CONCLUSIONS： Polydatin can delay renal fibrosis， the mechanism of which may be associated with up-regulating protein expression of MMP-9， down-regulating protein expression of TIMP-1 and increasing the ratio of MMP-9/TIMP-1.