Dihydromyricetin ameliorates hyperuricemia through inhibiting uric acid reabsorption.

BACKGROUND

Hyperuricemia (HUA) is a chronic disease caused by abnormal purine metabolism with high prevalence. Dihydromyricetin (DMY) is a natural flavonoid that is abundant in plants, such as vine tea, grapes and bayberry. DMY has been shown to possess multiple biological properties, but its anti-HUA effect remains underexplored. In the present study, the regulatory effects of DMY on HUA and its complications and mechanism were investigated.

RESULTS

DMY (10 and 20 μmol L-1) treatment significantly reduced xanthine oxidase (XOD) expression and uric acid (UA) synthesis in normal human liver cell strain cells, and intraperitoneal administration of DMY (100 mg kg-1) also significantly reduced serum UA and the expression of hepatic XOD in HUA mice. After DMY treatment for 12 consecutive days, the uricosuric protein, ATP-binding cassette subfamily G member 2, was upregulated, and reabsorption proteins, including urate transporter 1 and glucose transporter 9, were downregulated, which was consistent with the results of monosodium urate-induced HUA in human renal tubular epithelial cell line and human colon adenocarcinoma cell line cell models. In addition, DMY significantly ameliorated HUA-induced renal injury, and foot edema induced by monosodium urate. The nucleotide-binding oligomerization domain-like receptor family containing pyrin domain 3 (NLRP3) inflammasome was activated in HUA mice as evidenced by upregulation of NLRP3, caspase-1, ACS, TNF-α and IL-1β in the kidney and foot, which was significantly suppressed by DMY treatment.

CONCLUSION

Collectively, these findings suggested that DMY may play important roles in experimental HUA. © 2025 Society of Chemical Industry.