Sun Ze-Rui, Peng Hui-Zhen, Fan Mao-Si, Chang Dong, Wang Ming-Yue, An Meng-Fei, Zhang Li-Juan, Zan Rui, Sheng Jun, Zhao Yun-Li, Wang Xuan-Jun
College of Resources, Environment and Chemistry, Chuxiong Normal University, Chuxiong, China.
Key Laboratory of Pu-erh Tea Science, Ministry of Education, College of Science, College of Food Science and Technology, Yunnan Agricultural University, Kunming, China.
J Sci Food Agric. 2025 Jun;105(8):4178-4190. doi: 10.1002/jsfa.14126. Epub 2025 Apr 9.
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.
DMY (10 and 20 μmol L) 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) 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.
Collectively, these findings suggested that DMY may play important roles in experimental HUA. © 2025 Society of Chemical Industry.
高尿酸血症（HUA）是一种由嘌呤代谢异常引起的慢性疾病，患病率较高。二氢杨梅素（DMY）是一种天然黄酮类化合物，在植物中含量丰富，如藤茶、葡萄和杨梅。DMY已被证明具有多种生物学特性，但其抗HUA作用仍未得到充分研究。在本研究中，研究了DMY对HUA及其并发症的调节作用及其机制。
DMY（10和20μmol/L）处理显著降低了正常人肝细胞株细胞中黄嘌呤氧化酶（XOD）的表达和尿酸（UA）的合成，腹腔注射DMY（100mg/kg）也显著降低了HUA小鼠的血清UA和肝脏XOD的表达。连续12天给予DMY治疗后，尿酸排泄蛋白、ATP结合盒亚家族G成员2上调，而包括尿酸转运蛋白1和葡萄糖转运蛋白9在内的重吸收蛋白下调，这与尿酸钠诱导的人肾小管上皮细胞系和人结肠腺癌细胞系细胞模型中的HUA结果一致。此外，DMY显著改善了HUA诱导的肾损伤以及尿酸钠诱导的足部水肿。含吡咯结构域3（NLRP3）的核苷酸结合寡聚化结构域样受体家族炎性小体在HUA小鼠中被激活，肾脏和足部的NLRP3、半胱天冬酶-1、ACS、肿瘤坏死因子-α和白细胞介素-1β上调证明了这一点，而DMY治疗可显著抑制这种上调。
总的来说，这些发现表明DMY可能在实验性HUA中发挥重要作用。©2025化学工业协会。
