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

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

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Curcumin / administration & dosage*
  • Endothelial Cells / drug effects
  • Endothelial Cells / metabolism*
  • Fructose / adverse effects
  • Humans
  • Hyperuricemia / drug therapy*
  • Hyperuricemia / genetics
  • Hyperuricemia / metabolism
  • Janus Kinase 2 / genetics
  • Janus Kinase 2 / metabolism*
  • Kidney / cytology*
  • Kidney / drug effects
  • Kidney / metabolism
  • Male
  • Nitric Oxide / metabolism*
  • Plant Extracts / administration & dosage*
  • Protective Agents / administration & dosage*
  • Rats
  • Rats, Sprague-Dawley
  • STAT3 Transcription Factor / genetics
  • STAT3 Transcription Factor / metabolism*
  • Signal Transduction / drug effects*
  • Transforming Growth Factor beta1 / genetics
  • Transforming Growth Factor beta1 / metabolism

Substances

  • Plant Extracts
  • Protective Agents
  • STAT3 Transcription Factor
  • Transforming Growth Factor beta1
  • Fructose
  • Nitric Oxide
  • Janus Kinase 2
  • Curcumin