Genistein ameliorates hyperuricemia-associated nephropathy in hyperuricemic mice

Hyperuricemia is a metabolic disease caused by excessive production of uric acid (UA), which can cause gout, hypertension, hyperlipidemia and other diseases. This study aimed to explore the effect of genistein on hyperuricemia and renal protection in hyperuricemic mice induced by potassium oxonate. Furthermore, genistein significantly downregulated the xanthine oxidase (XOD), adenosine deaminase levels, renal gene expressions of glucose transporter type 9 (mGLUT9) and uric acid transporter 1 (mURAT1) and upregulated organic anion transporters (mOAT1 and mOAT3) and organic cation transporters (mOCT1 and mOCT2). Additionally, genistein improved renal function, renal histopathological features and antioxidant activities in hyperuricemic mice. Genistein also attenuated renal fibrosis by suppressing the JAK2/STAT3 and Wnt/beta-catenin signalling pathways in hyperuricemic mice. Overall, this study suggested that both doses of genistein have strong potential against hyperuricemia and associated disorders and may be used as natural supplements for the treatment of UA-related disorders.