Abstract
Rhizoma Dioscoreae Nipponicae, from Discorea nipponica, is a widely used traditional Chinese herb. It is used to treat arthroncus, arthrodynia, and arthritis. Hyperuricemia is an important foundation of gouty arthritis. The current study was aimed at investigating whether the effects of total saponins from Rhizoma Dioscoreae Nipponicae on hyperuricemia were due to renal organic ion transporters in potassium oxonate-induced hyperuricemia mice. Hyperplasia of synovial cells prepared from Wistar rats was induced by IL-1β (1 × 10(4) µg/mL). MTT was used and to screen active components in the inhibition of hyperplasia by total saponins from Rhizoma Dioscoreae Nipponica, individual pure compounds, and different combinations of these compounds. Sixty Kun Ming mice were randomly divided into six groups: normal, model, allopurinol (40 mg/kg), and three total saponins groups receiving dose (600 mg/kg), middle (300 mg/kg), and low doses (60 mg/kg). Hyperuricemic mice were induced with potassium oxonate (300 mg/kg) intragastrically. The total saponins were given six days and the positive drug allopurinol was given one day before inducing hyperuricemia. The serum and urine levels of uric acid and creatinine and the fractional excretion of uric acid were measured in normal and hyperuricemic mice treated with Rhizoma Dioscoreae Nipponicae and allopurinol. The mRNA and protein levels of the mouse urate transporter 1, glucose transporter 9, organic anion transporter 1, and organic anion transporter 3 were analyzed by real-time-PCR and Western blotting methods, respectively. Total saponins from Rhizoma Dioscoreae Nipponicae could effectively reverse potassium oxonate-induced alterations in renal mouse urate transporter 1, glucose transporter 9, organic anion transporter 1, and organic anion transporter 3 mRNA and protein levels, resulting in enhancement of renal urate excretion in mice. These findings suggested that the total saponins from Rhizoma Dioscoreae Nipponicae had a uricosuric effect on the regulation of renal organic ion transporters in hyperuricemic animals.
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