OBJECTIVE： To investigate the mechanism of the effects of apigenin on reducing uric acid and renal protection in oteracil potassium-induced hyperuricemia mice. METHODS： 50 mice were randomly divided into normal group， model group， allopurinol group （5 mg/kg）， apigenin low-dose and high-dose groups （40， 80 mg/kg）， with 10 mice in each group. Except for normal group， other groups were given oteracil potassium 250 mg/kg intragastrically to induce hyperuricemia model； 1 h after modeling， treatment groups were given relevant medicine intragastrically， and normal group and model group were given constant volume of normal saline intragastrically， once a day， for consecutive 7 d. Blood uric acid， urine uric acid and 24 h creatinine levels， the expression of kidney transporter associated protein （mURAT1， mOCT1， mOCT2， mOCTN1 and mOCTN2） were all determined in each group. RESULTS： Compared with normal group， blood uric acid， urine uric acid and mURAT1 levels of model group were significantly increased， while the expressions of mOCT1， mOCT2， mOCTN1 and mOCTN2， 24 h creatinine were significantly decreased （P＜0.01 or P＜0.001）. Compared with model group， blood uric acid， urine uric acid and mURAT1 levels of apigenin low-dose and high-dose groups， allopurinol group were significantly decreased， while 24 h creatinine， the expressions of mOCT1， mOCT2， mOCTN1 and mOCTN2 were increased significantly （P＜0.05 or P＜0.01 or P＜0.001）. CONCLUSIONS： Apigenin can reduce uric acid level of oteracil potassium-induced hyperuricemia mice and propect kidney， the mechanism of which may be associated with down-regulating the expression of mURAT1 and up-regulating the expressions of mOCTN1， mOCTN2， mOCT1 and mOCT2.