Protection of curcumin against fructose-induced hyperuricaemia and renal endothelial dysfunction involves NO-mediated JAK-STAT signalling in rats

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• 作者：Dong-Mei Zhang¹ ; Yu-Cheng Li¹ ; De Xu ; Xiao-Qin Ding ; Ling-Dong Kong ; ^{kongld@nju.edu.cn}
• 关键词：Curcumin ; Excess fructose consumption ; Anti-hyperuricaemic and renal protective actions ; Organic ion transporters ; Nitric oxide ; JAK2&ndash ; STAT3 signalling ; TGF-尾1
• 刊名：Food Chemistry
• 出版年：2012
• 期刊代码：48_03088146
• 类别：abs
• 出版时间：15 October, 2012
• 卷：134
• 期：4
• 页码：2184-2193
• 文件大小：1403 K

摘要

Increasing evidence has demonstrated that excess fructose consumption as a risk factor for metabolic syndrome causes hyperuricaemia and renal injury. Curcumin, a natural plant phenolic food additive, lowered serum urate, creatinine and blood urea nitrogen levels, and increased urinary urate and nitrate/nitrites levels, as well as renal nitric oxide (NO) production in fructose-fed rats. Moreover, curcumin regulated urate transport-related proteins and inhibited activation of the JAK2-STAT3 cascade and overexpression of SOCS3 and TGF-尾1 in the kidneys of fructose-fed rats. These results suggested that the anti-hyperuricaemic and renal protective actions of curcumin might be the result of renal NO-mediated JAK2-STAT3 signalling and TGF-尾1 normality, which ameliorated renal endothelial dysfunction to improve renal urate transporter system in this model. The present study may provide the evidence for the potential use of a functional food ingredient curcumin because of its action against hyperuricaemia and renal injury induced by high fructose intake.