Alleviation of Hyperuricemic Renal Injury Using Freeze-dried Cherry Juice Powder to Regulate Uric Acid Transporters
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Abstract:
A hyperuricemia (HUA) mouse model was developed through intraperitoneal injection of potassium oxonate for 7 days to investigate the potential of CJP in alleviating hyperuricemic renal injury by regulating uric acid transporters. After intervention in the HUA model using freeze-dried cherry juice powder (CJP), benzbromarone, and allopurinol, serum uric acid (UA), creatinine (Cr), and blood urea nitrogen (BUN) were detected using commercially available kits. Pathological changes in the liver and kidney were determined using hematoxylin-eosin (HE) staining. Expression of uric acid transporters in mouse kidney was assessed using western blot and immunohistochemistry. The UA level in the high-dose CJP group decreased from 191.99 to 113.12 μmol/L (P<0.01), remaining 25% higher than the normal level, whereas the Cr level decreased from 16.09 to 7.40 μmol/L (P<0.01), and the BUN level decreased from 8.24 to 4.73 mmol/L (P<0.01). The latter two indicators reached normal levels, demonstrating a substantial alleviation of renal tissue injury. CJP downregulated the expression of two uric acid-reabsorbing proteins, urate transporter 1 and glucose transporter 9, while upregulating the protein expression of three uric acid-secreting proteins, ATP-binding cassette superfamily G member 2, anion transporter 1, and anion transporter 3, with no obvious liver toxicity. CJP thus alleviates hyperuricemic renal injury by regulating uric acid transporters. This study can serve as a scientific basis for the development of health products derived from cherry for preventing and treating hyperuricemic renal injury.
