Abstract: OBJECTIVE To explore the effect and mechanism of licoflavonol(LCF) on reducing uric acid and inhibiting oxidative stress. METHODS The hyperuricemia cell model of renal tubular epithelial cells NRK-52E was induced by adenosine, 1.25, 5, and 20 μmol·L^-1 LCF were administered, then the contents of uric acid, hypoxanthine, xanthine, adenine, inosine and adenosine in the culture medium were detected by HPLC. NRK-52E cells were treated with 15 mg·dL^-1 uric acid to induce oxidative stress injury, 1.5, 5, and 15 μmol·L^-1 LCF were administrated respectively for 24 h, the activity of superoxide dismutase(SOD), catalase(CAT) and the contents of glutathione(GSH), malondialdehyde(MDA) and H₂O₂ in the cells were determined by kits. The binding activity of LCF to xanthine oxidase(XO) was predicted by molecular docking, and further investigated by microscale thermophoresis(MST). RESULTS LCF reduced the level of uric acid induced by adenosine, increased the activity of SOD and CAT and the content of GSH, decreased the content of H₂O₂ and MDA after uric acid induction. The molecular docking results showed that the binding energy between LCF and XO was -9.1 kcal·mol^-1, both were mainly formed hydrogen bonds, and the corresponding residues were Thr-262 and Glu-263. MST results showed that the dissociation constant Kd=(0.814 89±0.237 3)mmol·L^-1. CONCLUSION LCF can reduce the level of cellular uric acid induced by adenosine and improve the oxidative stress damage of renal tubular epithelial cells induced by high uric acid. Its mechanism of lowering uric acid may be related to XO.