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Vitamin C alleviates hyperuricemia nephropathy by reducing inflammation and fibrosis
Author(s) -
Li Hongling,
Liu Xuejiao,
Lee MeeHyun,
Li Haitao
Publication year - 2021
Publication title -
journal of food science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 150
eISSN - 1750-3841
pISSN - 0022-1147
DOI - 10.1111/1750-3841.15803
Subject(s) - hyperuricemia , xanthine oxidase , uric acid , medicine , endocrinology , nephropathy , febuxostat , vitamin c , fibrosis , kidney disease , vitamin d and neurology , gout , vitamin , kidney , chemistry , biochemistry , enzyme , diabetes mellitus
Hyperuricemia contributes to chronic kidney disease development. However, it has been historically viewed with limited research interest. In this study, we mimicked the development of hyperuricemic nephropathy by using a potassium oxonate‐induced hyperuricemia rat model. We found that administering vitamin C at 10 mg/kg/day effectively ameliorated hyperuricemic nephropathy. Compared to the control group, rats with hyperuricemia had significantly increased serum uric acid level, xanthine oxidase activity, and urine microalbumin level, by 5‐fold, 1.5‐fold, and 4‐fold, respectively. At the same time, vitamin C supplementation reverted these values by 20% for serum uric acid level and xanthine oxidase activity and 50% for microalbumin level. Vitamin C also alleviated renal pathology and decreased the expression of pro‐inflammatory and pro‐fibrotic markers. A further mechanistic study suggested that vitamin C might attenuate hyperuricemic nephropathy in renal tubular epithelial cells induced by monosodium urate (MSU) crystal, at least in part, by directly inhibiting IL‐6/JAK2/STAT3 signaling pathway. Meanwhile, in macrophages, vitamin C inhibited the expression of TGF‐β, and reduced ROS level induced by MSU by about 35%. In short, our results suggest that vitamin C supplementation delay the progression of hyperuricemic nephropathy.