{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T04:48:08Z","timestamp":1789534088687,"version":"build-2803163510"},"reference-count":39,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2025,4,9]],"date-time":"2025-04-09T00:00:00Z","timestamp":1744156800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["scijournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Sci Food Agric"],"published-print":{"date-parts":[[2025,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>BACKGROUND<\/jats:title><jats:p>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\u2010HUA effect remains underexplored. In the present study, the regulatory effects of DMY on HUA and its complications and mechanism were investigated.<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS<\/jats:title><jats:p>DMY (10 and 20\u2009\u03bcmol\u2009L<jats:sup>\u22121<\/jats:sup>) 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\u2009mg\u2009kg<jats:sup>\u22121<\/jats:sup>) 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\u2010binding 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\u2010induced HUA in human renal tubular epithelial cell line and human colon adenocarcinoma cell line cell models. In addition, DMY significantly ameliorated HUA\u2010induced renal injury, and foot edema induced by monosodium urate. The nucleotide\u2010binding oligomerization domain\u2010like receptor family containing pyrin domain 3 (NLRP3) inflammasome was activated in HUA mice as evidenced by upregulation of NLRP3, caspase\u20101, ACS, TNF\u2010<jats:italic>\u03b1<\/jats:italic> and IL\u20101<jats:italic>\u03b2<\/jats:italic> in the kidney and foot, which was significantly suppressed by DMY treatment.<\/jats:p><\/jats:sec><jats:sec><jats:title>CONCLUSION<\/jats:title><jats:p>Collectively, these findings suggested that DMY may play important roles in experimental HUA. \u00a9 2025 Society of Chemical Industry.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jsfa.14126","type":"journal-article","created":{"date-parts":[[2025,4,9]],"date-time":"2025-04-09T05:27:10Z","timestamp":1744176430000},"page":"4178-4190","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Dihydromyricetin ameliorates hyperuricemia through inhibiting uric acid reabsorption"],"prefix":"10.1002","volume":"105","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0511-5304","authenticated-orcid":false,"given":"Ze\u2010Rui","family":"Sun","sequence":"first","affiliation":[{"name":"College of Resources, Environment and Chemistry, Chuxiong Normal University  Chuxiong China"},{"name":"Key Laboratory of Pu\u2010erh Tea Science, Ministry of Education College of Science, College of Food Science and Technology, Yunnan Agricultural University  Kunming China"},{"name":"College of Food Science and Technology, Nanjing Agricultural University  Nanjing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui\u2010Zhen","family":"Peng","sequence":"additional","affiliation":[{"name":"School of Chinese Materia Medica and Yunnan Key Laboratory of Southern Medicinal Resource, School of Basic Medicine, Yunnan University of Chinese Medicine  Kunming 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