Chicory (Cichorium intybus L.) inhibits renal reabsorption by regulating expression of urate transporters in fructose-induced hyperuricemia

Abstract

Objective: Hyperuricemia is an excess of urate in blood. The kidneys play important parts in urate excretion, which involves handling reabsorption and secretion. A series of urate transporters is responsible for this process: urate transporter (URAT)1, glucose transporter (GLUT)9, organic anion transporter (OAT)1 and OAT3. Excessive fructose intake may result in increased serum urate levels. Chicory (Cichorium intybus L.) has been used as an edible vegetable and traditional Chinese medicine. Studies have shown that chicory is a promising anti-hyperuricemia agent and we explored the mechanism of its uricosuric effect via a renal pathway. Methods: Hyperuricemia was induced in rats by administration of 10% fructose. The uricosuric effect was evaluated by determining the serum urate level. Renal excretory function was detected by the clearance rate of creatinine, clearance rate of uric acid and histology. The location and expression of URAT1, GLUT9, OAT1 and OAT3 their mRNA expression in kidneys were analyzed. Results: Chicory decreased serum levels of urate and creatinine significantly, and promoted the clearance of creatinine and urate, as well as improving renal pathologic changes due to hyperuricemia. Chicory inhibited expression of URAT1 and GLUT9 markedly in a dose-dependent manner, but showed no influence on expression of OAT1 or OAT3. Conclusion: Chicory might be a promising anti-hyperuricemia agent. It can promote renal excretion of urate by inhibiting urate reabsorption, which may be related to down-regulation of mRNA and protein expression of URAT1 and GLUT9. Keywords: Chicory, Fructose, Hyperuricemia, Renal resorption, Urate transporters