Abstract
Purpose: To investigate the anti-hyperuricemic effect of Dioscorea tokoro Makino extract (DTME) in potassium oxonate-induced hyperuricemic mice.Method: The effect of DTME was investigated in the hyperuricemic mice induced by potassium oxonate. DTME. The extract was administered to the mice daily at doses of 220, 440 and 880 mg/kg for 10 days; allopurinol (5 mg/kg) was given as positive control. Serum and urine levels of uric acid and creatinine were determined by colorimetric method. Simultaneously, protein levels of urate transporter 1 (URAT1) and organic anion transporter 1 (OAT1) in the rat kidney were analyzed by Western blotting.Results: Compared with control, a high dose of DTME inhibited xanthine oxidase (XOD) activity in both serum (18.12 ± 1.33 U/L) and in liver (70.15 ± 5.20 U/g protein) (p < 0.05); decreased levels of serum uric acid (2.04 ± 0.64 mg/L) (p < 0.05), serum creatinine (0.35 ± 0.18 μmol/L) and blood urea nitrogen (BUN) (8.83 ± 0.71 mmol/L) (p < 0.05). Furthermore, the extract increased levels of urine uric acid (38.34 ± 8.23 mg/L), urine creatinine (34.38 ± 1.98 mmol/L), down regulated of URAT1 and up regulated of OAT1 protein expressions (p < 0.05) in the renal tissue of hyperuricemic mice.Conclusion: DTME improves renal dysfunction in rats by regulating renal urate transporters in hyperuricemic rats. This may find therapeutic application in antihypertensive therapy.Keywords: Dioscorea tokoro Makino, Hyperuricemic, Renal urate transporters, Uric acid, Creatinine
Highlights
Hyperuricemia is one of the most common and extensive metabolic diseases in populations, characterized by high uric acid level in the blood, causing deposition of urate crystals in the joints and kidneys, and is well known as important risk factor for gouty arthritis, uric acid nephrolithiasis, cardiovascular and renal disease, especially hypertension [1,2]
This study is to investigate therapeutic effects of Dioscorea tokoro Makino extract (DTME) on xanthine oxidase (XOD) activity and urate excretion in experimental hyperuricemia mice
The major regulator of serum uric acid (SUA) is renal excretion of uric acid. This renal exchange is mediated by specialized molecules expressed in renal proximal tubule cells, in which Urate transporter 1 (URAT1) and organic anion transporter 1 (OAT1) have been considered to play an important role in UA handling [13]
Summary
Hyperuricemia is one of the most common and extensive metabolic diseases in populations, characterized by high uric acid level in the blood, causing deposition of urate crystals in the joints and kidneys, and is well known as important risk factor for gouty arthritis, uric acid nephrolithiasis, cardiovascular and renal disease, especially hypertension [1,2]. Despite advances in the use of anti-hyperuricemic agents for the treatment of hyperuricaemia and gout, allopurinol as a frequently used xanthine oxidase (XOD) inhibitor could induce severe hypersensitivity (such as a mild exanthema) and agranulocytosis, and aggravate renal toxicity by impairing pyrimidine metabolism [3,4]. It is necessary to study available anti-hyperuricemic agents, especially herbal medicine [5]. This study is to investigate therapeutic effects of DTME on XOD activity and urate excretion in experimental hyperuricemia mice.
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