curcumin and Hyperuricemia

Hyperuricemia leads to gout and renal complications and may increase cardiovascular risk. Curcumin inhibits xanthine oxidase and increases uricosuric activity and, as a result, decreases serum urate (SU). This randomized controlled trial aimed to determine the effects of curcumin versus placebo on SU in subjects with asymptomatic hyperuricemia (SU level ≥ 6 mg/dL in women or ≥ 7 mg/dL in men).. Thirty-nine subjects with persistent hyperuricemia were randomized to receive curcumin (500-mg capsules twice daily, 20 subjects) or placebo (19 subjects). Primary outcome was the difference between SU before and 8 weeks after randomization. Secondary outcomes were differences between urine uric acid (UUA) clearance, fasting plasma glucose (FPG), and lipid profiles before and 8 weeks after randomization and adverse events.. Out of 39 subjects, there were no differences at baseline SU, UUA clearance, FPG, lipid profiles, and demographics between curcumin and placebo groups. After 8 weeks, SU was significantly decreased in both groups (6.9% in curcumin group,. Curcumin was not superior to placebo in reducing serum urate and in increasing UUA clearance.

Topics: Curcumin; Female; Gout; Humans; Hyperuricemia; Male; Treatment Outcome; Uric Acid

Current evidences suggest that hyperuricemia is closely related to the overproduction or underexcretion of uric acid (UA). Curcumin (CUR), a natural polyphenol component extracted from the rhizome of Curcuma longa, has been reported to treat various symptoms such inflammation disease, seems to be efficacious in hyperuricemia. In this study, we aimed to investigate the effect of CUR on hyperuricemia and kidney inflammation in hyperuricemic mice. Administration with CUR (20 or 40 mg/kg) or allopurinol (ALL, 5 mg/kg) was given to mice orally one hour later after the injection of potassium oxonate (PO) (300 mg/kg, i.p.) for 14 days. CUR administration decreased the levels of uric acid (UA), creatinine (CRE) and blood urea nitrogen (BUN) in serum. Meanwhile, treatment with CUR effectively inhibited serum and liver xanthine oxidase (XOD) levels, and further renewed normal antioxidant enzymes activities (SOD, GSH-Px), reduced MDA accumulation in serum. Further studies showed that CUR decreased inflammatory cytokines productions (IL-1β, IL-18) in serum, as well as inhibited PO-induced the activation of NLRP3 inflammasome signaling in the kidney. In conclusion, the study revealed that CUR exhibited anti-hyperuricemic and anti-inflammatory effects through suppressing NLRP3 inflammasome activation in kidney and provided the evidence for treating hyperuricemia and associated renal inflammation.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Biomarkers; Curcumin; Cytokines; Disease Models, Animal; Hyperuricemia; Inflammasomes; Inflammation; Kidney; Kidney Function Tests; Male; Mice, Inbred Strains; NLR Family, Pyrin Domain-Containing 3 Protein; Oxonic Acid

A series of curcumin derivatives as potent dual inhibitors of xanthine oxidase (XOD) and urate transporter 1 (URAT1) was discovered as anti-hyperuricemic agents. These compounds proved efficient effects on anti-hyperuricemic activity and uricosuric activity in vivo. More importantly, some of them exhibited proved efficient effects on inhibiting XOD activity and suppressing uptake of uric acid via URAT1 in vitro. Especially, the treatment of 4d was demonstrated to improve uric acid over-production and under-excretion in oxonate-induced hyperuricemic mice through regulating XOD activity and URAT1 expression. Docking study was performed to elucidate the potent XOD inhibition of 4d. Compound 4d may serve as a tool compound for further design of anti-hyperuricemic drugs targeting both XOD and URAT1.

Topics: Animals; Curcumin; Enzyme Inhibitors; HEK293 Cells; Humans; Hyperuricemia; Male; Mice; Models, Molecular; Organic Anion Transporters; Organic Cation Transport Proteins; Uric Acid; Xanthine Oxidase

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.

Topics: Animals; Curcumin; Endothelial Cells; Fructose; Humans; Hyperuricemia; Janus Kinase 2; Kidney; Male; Nitric Oxide; Plant Extracts; Protective Agents; Rats; Rats, Sprague-Dawley; Signal Transduction; STAT3 Transcription Factor; Transforming Growth Factor beta1