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.