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Food Chem. 2012 Oct 15;134(4):2184-93. doi: 10.1016/j.foodchem.2012.04.026. Epub 2012 Apr 17.

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

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1
State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing 210093, PR China.

Abstract

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-β1 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-β1 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.

PMID:
23442673
DOI:
10.1016/j.foodchem.2012.04.026
[Indexed for MEDLINE]

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