Quercetin ameliorates hyperuricemic nephropathy by repressing uric acid synthesis and reabsorption in mice and cells
Wenhui Li,
Xuerui Chen,
Feng Li,
Zhang Huiyao,
Zunyang Song,
Dapeng Li
Affiliations
Wenhui Li
College of Food Science and Engineering, Key Laboratory of Food Nutrition and Human Health in Universities of Shandong Shandong Agricultural University Taian People's Republic of China
Xuerui Chen
College of Food Science and Engineering, Key Laboratory of Food Nutrition and Human Health in Universities of Shandong Shandong Agricultural University Taian People's Republic of China
Feng Li
College of Food Science and Engineering, Key Laboratory of Food Nutrition and Human Health in Universities of Shandong Shandong Agricultural University Taian People's Republic of China
Zhang Huiyao
College of Food Science and Engineering, Key Laboratory of Food Nutrition and Human Health in Universities of Shandong Shandong Agricultural University Taian People's Republic of China
Zunyang Song
College of Food Science and Engineering, Key Laboratory of Food Nutrition and Human Health in Universities of Shandong Shandong Agricultural University Taian People's Republic of China
Dapeng Li
College of Food Science and Engineering, Key Laboratory of Food Nutrition and Human Health in Universities of Shandong Shandong Agricultural University Taian People's Republic of China
Abstract Hyperuricemia as one of the key factors for gout, and quercetin could reduce the uric acid (UA) content. However, the mechanism of quercetin reduces UA content is still uncovered. Herein, we found quercetin can reduce UA content, induce antioxidant enzyme activity, inhibit the enzyme activity of xanthine oxidase (XOD) in hyperuricemia mice. Moreover, the UA reabsorption was also significantly reduced in the kidney and the kidney inflammation was alleviated by quercetin in hyperuricemia mice. Meanwhile, the protein level of ATP‐binding cassette super‐family G member 2 (ABCG2) was markedly induced and the protein levels of urate transporter 1 (URAT1) and glucose transporter 9 (GLUT9) were significantly repressed by quercetin in hyperuricemia mice and HK‐2 cells and by quercetin‐3‐O‐glucuronide in HK‐2 cells. Additionally, the docking mode indicated that quercetin is stable bound to the active site of XOD. Overall, the data reveal that quercetin alleviates hyperuricemia by repressing the activity of XOD, reducing the UA absorption via enhancing ABCG2 expression, and repressing URAT1 and GLUT9 expression.