Hyperuricemia (HUA) is a universal metabolic disorder characterized by a high level of uric acid in the serum. Anthocyanins (ACNs) are a group of natural flavonoids that have shown favourable bioactivities in the metabolic syndrome but the effect on uric acid metabolism remains underexplored. The present study investigated the hypouricemic effects of ACNs in a mice model and further studied the potential mechanisms. ICR mice based on a high-yeast diet were administered potassium oxonate (PO, 280 mg per kg body weight) and inosine (400 mg per kg body weight) to induce a hyperuricemia model, meanwhile, ACNs were supplemented by gavage. The mice were sacrificed after 3 weeks of treatment. ACN administration significantly reduced serum uric acid (SUA), blood urea nitrogen (BUN) and serum creatinine (Scr) levels and suppressed xanthine oxidase (XOD) activity in mice serum and liver. In addition, ACNs down-regulated the expression of hepatic XOD, caspase-1, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) and regulated the expression of renal urate transporters URAT1, GLUT9, ABCG2, OAT1, OAT3, OCT1, OCT2, OCTN1 and OCTN2. According to histological analysis, ACN treatment exhibited hepatoprotective and nephroprotective effects in hyperuricemic mice. In conclusion, ACNs reduced urate production and promoted uric acid excretion from the renal system, which suggests the potential of ACNs for the future treatment of HUA.