Anti-Hyperuricemic Effects of Ampelopsis grossedentata Extract and Its Major Component Dihydromyricetin via Targeted Regulation of Uric Acid Metabolism

Hyperuricemia (HUA), a prevalent metabolic disorder, is increasingly recognized as a critical contributor to the onset and progression of various chronic diseases, including cardiovascular and renal conditions. However, the adverse effects and long-term dependence associated with conventional pharmacological therapies highlight the pressing need for safe and effective nutritional interventions. This study systematically investigated the anti-hyperuricemic potential of an ethanol extract of Ampelopsis grossedentata (AMP) and its principal flavonoid, dihydromyricetin (DMY), through integrated in vitro and in vivo approaches. In the mouse model of HUA, AMP (125, 500 mg/kg) thine oxidase (XOD) activity and modulation of key urate transporters, including GLUT9, URAT1, and ABCG2. Phytochemical profiling revealed that DMY accounts for 52.97% of the total flavonoids in AMP. Further mechanistic studies demonstrated that DMY (50, 100, 200 mg/kg) exerted dose-dependent inhibition of XOD activity, regulated the expression of urate transporter genes, and protected renal tubular cells from uric acid-induced cytotoxicity. Collectively, AMP displays multi-targeted regulatory effects on uric acid metabolism, with DMY identified as its core bioactive constituent. These findings offer new insights into the molecular mechanisms of natural flavonoids in managing uric acid homeostasis and support the development of A. grossedentata-derived functional ingredients as promising nutritional strategies for hyperuricemia prevention and therapy.