Institute of Food Science and Technology, Fujian Academy of Agricultural Sciences, Fuzhou 350003, China.
National R & D Center for Edible Fungi Processing, Fuzhou 350003, China.
Food Funct. 2024 Aug 27;15(17):8823-8834. doi: 10.1039/d4fo02391a.
The incidence of hyperuricemia (HUA) shows a gradually increasing trend towards affecting younger individuals, and it can significantly harm the overall health status of the body. Based on a metabolomics perspective, this study reveals the mechanism of the uric acid-lowering action of Lindl. cv. "furong" polyphenols (PSLP) on a hyperuricemia mouse model induced by hypoxanthine and potassium oxybutyrate. The results demonstrate that PSLP comprise an effective treatment strategy for reducing the levels of serum uric acid (SUA), serum creatinine (SCr) and blood urea nitrogen (BUN) in HUA mice ( < 0.05), wherein the maximum decrease rates are up to 44.50%, 29.46%, and 32.95%, respectively. PSLP are observed to exert a pronounced inhibitory effect on the activities of xanthine oxidase (XOD) and adenosine deaminase (ADA) in the livers of HUA mice, with reductions of up to 16.36% and 20.13%, respectively. These findings illustrate that PSLP exert a significant uric acid-lowering effect. Subsequent metabolomic analysis of mouse serum identified 28 potential biomarkers for hyperuricemia, whose levels were markedly diminished by PSLP. This process involved alterations in purine, glycine, the pentose phosphate pathway, and galactose metabolism. Twenty-eight potential biomarkers were identified for hyperuricemia by subsequent metabolomic analysis of mouse serum, whose levels were markedly reversed by PSLP intervention. The regulation of HUA by PSLP involved alterations in purine metabolism, glycerolipid metabolism, the pentose phosphate pathway, and galactose metabolism. The mechanism of PSLP ameliorated hyperuricemia might be attributed to reduction of the level of the uric acid precursor ribose-5-phosphate in the pentose phosphate pathway, the inhibition of the activities of uric acid synthase XOD and ADA in purine metabolism, and reduction of the synthesis of the end product uric acid. This study provides a theoretical basis for the development of functional foods based on PSLP, which can potentially reduce uric acid levels.
高尿酸血症（HUA）的发病率呈逐渐年轻化趋势，对机体整体健康状况危害较大。基于代谢组学角度，揭示了芙蓉李多酚（PSLP）降低次黄嘌呤和氧代丁酸钾诱导的高尿酸血症模型小鼠血尿酸（SUA）、血清肌酐（SCr）和血尿素氮（BUN）水平的作用机制。结果表明，PSLP 可有效降低 HUA 小鼠的血清尿酸（SUA）、血清肌酐（SCr）和血尿素氮（BUN）水平（ < 0.05），最大降幅分别可达 44.50%、29.46%和 32.95%；PSLP 对 HUA 小鼠肝脏黄嘌呤氧化酶（XOD）和腺苷脱氨酶（ADA）活性有明显的抑制作用，降幅分别可达 16.36%和 20.13%；说明 PSLP 具有显著的降尿酸作用。随后对小鼠血清进行代谢组学分析，鉴定出 28 个潜在的高尿酸血症生物标志物，PSLP 可显著降低其水平。该过程涉及嘌呤、甘氨酸、戊糖磷酸途径和半乳糖代谢的改变。随后对小鼠血清进行代谢组学分析，鉴定出 28 个潜在的高尿酸血症生物标志物，PSLP 可显著降低其水平。PSLP 调节 HUA 涉及嘌呤代谢、甘油磷脂代谢、戊糖磷酸途径和半乳糖代谢的改变。PSLP 改善高尿酸血症的机制可能归因于降低戊糖磷酸途径中尿酸前体核糖-5-磷酸的水平，抑制嘌呤代谢中尿酸合酶 XOD 和 ADA 的活性，减少尿酸终产物的合成。该研究为基于 PSLP 开发降尿酸功能食品提供了理论依据。
