Abstract Title:

Anti-hyperuricemic and nephroprotective effects of Modified Simiao Decoction in hyperuricemic mice.

Abstract Source:

J Ethnopharmacol. 2012 Jun 26 ;142(1):248-52. Epub 2012 May 8. PMID: 22575704

Abstract Author(s):

Jian Hua, Ping Huang, Chong-Mei Zhu, Xiao Yuan, Chen-Huan Yu

Article Affiliation:

The Second People Hospital of Xihu District, Hangzhou 310024, China.


ETHNOPHARMACOLOGICAL RELEVANCE: Modified Simiao Decoction (MSD), based on clinical experience, has been used for decades and famous for its efficiency in treating hyperuricemic and gouty diseases.

AIM OF THE STUDY: To investigate the effects of MSD on anti-hyperuricemic and nephroprotective effects are involved in potassium oxonate-induced hyperuricemic mice.

MATERIALS AND METHODS: The effects of MSD were investigated in hyperuricemic mice induced by potassium oxonate. MSD were fed to hyperuricemic mice daily at a dose of 0.45, 0.90, 1.80 g/kg for 10 days, and allopurinol (5mg/kg) was given as a positive control. Serum and urine levels of uric acid and creatinine, and fractional excretion of uric acid (FEUA) were determined by colorimetric method. Its nephroprotective effects were evaluated by determining a panel of oxidative stress markers after the intervention in hyperuricemic mice. Simultaneously, protein levels of urate transporter 1 (URAT1) and organic anion transporter 1 (OAT1) in the kidney were analyzed by Western blotting.

RESULTS: MSD could inhibit XOD activities in serum and liver, decrease levels of serum uric acid, serum creatinine and BUN, and increased levels of urine uric acid, urine creatinine, FEUA dose-dependently through down-regulation of URAT1 and up-regulation of OAT1 protein expressions in the renal tissue of hyperuricemic mice. It also effectively reversed oxonate-induced alterations on renal MDA levels and SOD activities in this model.

CONCLUSION: MSD processes uricosuric and nephroprotective actions by regulating renal urate transporters and enhancing antioxidant enzymes activities to improve renal dysfunction in hyperuricemic mice.

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Sayer Ji
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