The effects of mangiferin on uric acid excretion, kidney function and related renal transporters were investigated in hyperuricemic mice induced by potassium oxonate.  Mice were divided into normal control group, and 5 hyperuricemic groups with model control, 50, 100, and 200 mg·kg⁻¹ mangiferin, and 5 mg·kg⁻¹   allopurinol.  Mice were administered by gavage once daily with 250 mg·kg⁻¹ potassium oxonate for seven   consecutive days to create the model.  And 3 doses of mangiferin were orally initiated on the day 1 h after   potassium oxonate was given, separately.  Serum uric acid, creatinine and urea nitrogon levels, as well as   urinary uric acid creatinine levels were measured.  Mouse uromodulin (mUMOD) levels in serum, urine    and kidney were determined by ELISA method.  The mRNA and protein levels of related renal transporters were assayed by RT-PCR and Western blotting methods, respectively.  Compared to model group, mangiferin significantly reduced serum uric acid, creatinine and urea nitrogon levels, increased 24 h uric acid and    creatinine excretion, and fractional excretion of uric acid in hyperuricemic mice, exhibiting uric acid excretion enhancement and kidney function improvement.  Mangiferin was found to down-regulate mRNA and protein levels of urate transporter 1 (mURAT1) and glucose transporter 9 (mGLUT9), as well as up-regulate organic  anion transporter 1 (mOAT1) in the kidney of hyperuricemic mice.  These findings suggested that mangiferin might enhance uric acid excretion and in turn reduce serum uric acid level through the decrease of uric acid   reabsorption and the increase of uric acid secretion in hyperuricemic mice.  Moreover, mangiferin remarkably up-regulated expression levels of renal organic cation and carnitine transporters (mOCT1, mOCT2, mOCTN1 and mOCTN2), increased urine mUMOD levels, as well as decreased serum and kidney mUMOD levels in   hyperuricemic mice, which might be involved in mangiferin-mediated renal protective action.