Abstract

Tabebuia species (Bignoniaceae) have long been used in folk medicine as anti-inflammatory, antirheumatic, antimicrobial, and antitumor. The aim of this study was to investigate if aqueous extract from the leaves (AEL) of Tabebuia roseoalba (Ridl.) Sandwith, Bignoniaceae, and its constituents could be useful to decrease serum uric acid levels and restrain the gout inflammatory process. HPLC analysis identified caffeic acid and chlorogenic acid in AEL. Antihyperuricemic effects and inhibition of liver XOD (xanthine oxidoreductase) by AEL and identified compounds were evaluated in hyperuricemic mice. Anti-inflammatory activity was evaluated on MSU (monosodium urate) crystal-induced paw edema. In addition, AEL antioxidant activity in vitro was evaluated. AEL, caffeic, and chlorogenic acids were able to reduce serum uric acid levels in hyperuricemic mice probably through inhibition of liver xanthine oxidase activity and significantly decreased the paw edema induced by MSU crystals. AEL showed significant antioxidant activity in all evaluated assays. The results show that the AEL of Tabebuia roseoalba can be a promising agent for treatment for gout and inflammatory diseases. We suggest that caffeic and chlorogenic acids may be responsible for the activities demonstrated by the species.

Highlights

  • More than 200 years ago, hyperuricemia is known to be causally involved in the pathogenesis of gout, a painful inflammatory arthritis induced by the deposition of monosodium urate (MSU) crystals in synovial fluid and other tissues [1]

  • The final product of purine metabolism in human is uric acid and it is generated by the action of xanthine oxidase (XO) enzyme, which catalyzes the conversion of hypoxanthine to xanthine and of xanthine to uric acid [3]

  • Analyses carried on HPLCUV/DAD comparing retention time and UV spectra with standards confirmed the presence in aqueous extract from the leaves (AEL) of caffeic

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Summary

Introduction

More than 200 years ago, hyperuricemia is known to be causally involved in the pathogenesis of gout, a painful inflammatory arthritis induced by the deposition of monosodium urate (MSU) crystals in synovial fluid and other tissues [1]. Current acute gout treatment focuses on controlling pain and inflammation. Drugs such as colchicine, NSAIDs (nonsteroidal anti-inflammatory drugs), and analgesics are part of the therapeutic regime for gout. Once the acute crisis is controlled, drugs that reduce uric acid are prescribed. These drugs include allopurinol, which inhibit uric acid production, benzbromarone and probenecid, which increase its renal excretion [2, 4]. These drugs are known to cause severe gastrointestinal, renal, and cardiovascular adverse effects [5]. The development of a new effective and safety antihyperuricemic and anti-inflammatory drug could be useful in gout therapy and is highly justified

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