Modified Chuanhu anti-gout mixture, a traditional Chinese medicine, protects against potassium oxonate-induced hyperuricemia and renal dysfunction in mice. Issue 5 (May 2019)

• Record Type: Journal Article
• Authors: You, Wenjun; Wang, Jie; Zou, Yaowu; Che, Kui; Hou, Xu; Fei, Honghua; Wang, Yangang
• Is Part Of: Journal of international medical research. Volume 47:Issue 5(2019)
• Page Start: 1927
• Page End: 1935
• Publication Date: 2019-05
• Subjects: Chuanhu anti-gout mixture -- hyperuricemia -- renal dysfunction -- traditional Chinese medicine -- xanthine oxidase -- urate transporter 1; Medicine -- Periodicals; Pharmacology -- Periodicals; 610.5
• DOI: 10.1177/0300060519831182
• Languages: English
• ISSNs: 0300-0605

Abstract

Objective: Acute gout is a painful, inflammatory arthritis that features a rapidly escalating inflammatory response resulting from the formation of monosodium urate crystals in the affected joint space. Previously, we found that Chuanhu anti-gout mixture (CAGM) had similar effects as colchicine against gout in the clinic. Subsequently, to improve its effectiveness and efficacy, we modified the original formulation of CAGM. The current study evaluated the effectiveness of the modified formulation in mice. Methods: Potassium oxonate (PO) was used to establish a mouse model of hyperuricemia. Plasma levels of uric acid and creatine were determined using the respective test kits. Hepatic xanthine oxidase (XOD) expression was examined by enzyme-linked immunosorbent assay. To explore the underlying mechanism, renal urate transporter 1 (URAT1) mRNA levels were evaluated by quantitative real-time PCR. Allopurinol and benzbromarone were used as reference drugs. Results: The original CAGM and its modified high-dose formulation significantly reduced serum uric acid and creatine levels in hyperuricemic mice. In addition, the CAGM-treated groups displayed lower mRNA levels of hepatic XOD and renal URAT1. Conclusions: CAGM and its modified formulation significantly ameliorated PO-induced hyperuricemia in mice, which might be partially attributable to reductions of hepatic XOD and renal URAT1 levels.