ArticleAmerican journal of translational research2025
Multi-target mechanism of 6-O-Caffeoylarbutin in hyperuricemia treatment through
Article in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo evaluate the therapeutic effects of 6-O-Caffeoylarbutin on hyperuricemia (HUA) and renal inflammation in a mouse model and explore its underlying multi-target mechanisms.
methodsA HUA mouse model was established using potassium oxonate and hypoxanthine. Mice were treated with 6-O-Caffeoylarbutin (100, 200, 300 mg/kg) or benzbromarone (10 mg/kg) for 14 days. Serum uric acid (SUA), creatinine, and xanthine oxidase (XOD) levels were measured. Renal injury and inflammation were assessed by H&E staining and ELISA for IL-1β, TNF-α, and IL-6. Network pharmacology and molecular docking predicted potential targets, which were validated by western blotting (WB).
resultsBoth 6-O-Caffeoylarbutin and benzbromarone significantly reduced renal tissue damage, tubular dilation, and interstitial edema by routine histology. In HUA mice, they also lowered SUA levels. ELISA showed significant reductions in IL-1β, TNF-α, and IL-6, indicating anti-inflammatory effects. Notably, the high-dose 6-O-Caffeoylarbutin group showed results comparable to benzbromarone. Network pharmacology identified six putative targets related to uric acid metabolism and inflammation, with molecular docking confirming stable binding. WB confirmed regulatory activity, showing reduced expression of XDH, SERPINE1, ALB, SLC37A4, SLC28A2, and HPRT1.
conclusion6-O-Caffeoylarbutin effectively reduces uric acid levels and alleviates renal inflammation in HUA mice through multi-target mechanisms, including inhibition of urate production, promotion of excretion, and anti-inflammatory activity. It shows promise as a natural therapeutic candidate for HUA.
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