[Anti-hyperuricemia effect and mechanism of polydatin in mice]

Area of Science:

• Pharmacology
• Nephrology
• Biochemistry

Background:

• Hyperuricemia is a condition characterized by elevated serum uric acid levels.
• Uricase inhibitors like potassium oxonate are used to induce hyperuricemia in animal models.
• Kidney transporters, including urate anion transporter 1 (URAT1), organic anion transporter 1 (OAT1), and organic anion transporter 3 (OAT3), play crucial roles in uric acid excretion.

Purpose of the Study:

• To investigate the effect of polydatin on serum uric acid levels in a hyperuricemia mice model.
• To examine the impact of polydatin on the gene expression of kidney transporters URAT1, OAT1, and OAT3.
• To compare the efficacy of polydatin with benzbromarone, a known uricosuric agent.

Main Methods:

• A hyperuricemia mice model was established using potassium oxonate.
• Mice were treated with varying doses of polydatin (5, 10, 20 mg/kg) or benzbromarone (16.7 mg/kg) for seven days.
• Serum uric acid levels were measured.
• Real-time PCR was employed to quantify the gene expression of URAT1, OAT1, and OAT3 in kidney tissues.

Main Results:

• Both polydatin and benzbromarone significantly reduced serum uric acid levels in hyperuricemia mice compared to the model group (P < 0.05).
• Hyperuricemia significantly altered the expression of URAT1, OAT1, and OAT3 in the kidneys compared to the control group (P < 0.05).
• Polydatin demonstrated a dose-dependent inhibition of the potassium oxonate-induced changes in these transporter genes (P < 0.05).

Conclusions:

• Polydatin effectively reduces serum uric acid levels in a mouse model of hyperuricemia.
• The mechanism involves the modulation of kidney transporters URAT1, OAT1, and OAT3, promoting uric acid excretion.
• Polydatin shows potential as a therapeutic agent for managing hyperuricemia.