Planta Med 2006; 72(7): 584-589
DOI: 10.1055/s-2006-931564
Original Paper
Pharmacology
© Georg Thieme Verlag KG Stuttgart · New York

12-Acetoxyhawtriwaic Acid Lactone, a Diterpene from Egletes viscosa, Attenuates Capsaicin-Induced Ear Edema and Hindpaw Nociception in Mice: Possible Mechanisms

Caroline M. Melo1 , Juliana L. Maia1 , Ítalo J. M. Cavalcante1 , Mary Anne S. Lima2 , Gizelle Angela B. Vieira2 , Edilberto R. Silveira2 , Vietla S. N. Rao1 , Flávia A. Santos1
  • 1Department of Physiology and Pharmacology, Federal University of Ceará, Fortaleza, CE, Brazil
  • 2Department of Organic and Inorganic Chemistry, Federal University Ceará, Fortaleza, CE, Brazil
Further Information

Publication History

Received: September 15, 2005

Accepted: December 30, 2005

Publication Date:
24 April 2006 (online)

Abstract

The diterpene, 12-acetoxyhawtriwaic acid lactone (AHAL, tanabalin) isolated from the flower buds of Egletes viscosa Less. (Asteraceae) was evaluated on capsaicin-induced ear edema and hindpaw nociception in mice. AHAL (12.5, 25 and 50 mg/kg, p. o.) significantly attenuated the ear edema response to topically applied capsaicin (250 μg), in a dose-related manner. At similar doses, AHAL also suppressed the nocifensive paw-licking behavior induced by intraplantar injection of capsaicin (1.6 μg). These responses to capsaicin were also greatly inhibited by ruthenium red (3 mg/kg, s. c.), a non-competitive capsaicin receptor (TRPV1) antagonist. The anti-edema effect of AHAL (50 mg/kg) seems unrelated to either blockade of mast cell degranulation or to histamine and serotonin receptor antagonism since AHAL did not modify the paw edema response induced by intraplantar injections of compound 48/80, histamine or serotonin. However, the hindpaw edema induced by substance P and vascular permeability increase induced by intraperitoneal acetic acid were significantly suppressed by AHAL. The antinociceptive effect of AHAL (50 mg/kg) was unaffected by naloxone pretreatment but was significantly antagonized by theophylline and glibenclamide, the respective blockers of adenosine and KATP-channels. AHAL (50 mg/kg, p. o.) did not impair the ambulation or motor coordination of mice in open-field and rota-rod tests. These data suggest that AHAL inhibits acute neurogenic inflammation possibly involving capsaicin-sensitive TRPV1-receptors, endogenous adenosine and ATP-sensitive potassium channels.

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Flavia A. Santos, PhD

Departamento de Fisiologia e Farmacologia

Universidade Federal do Ceará

Rua Cel Nunes de Melo-1127

Caixa Postal-3157

60430-270 Fortaleza, CE

Brasil

Phone: +55-85-4009-8341

Fax: +55-85-4009-8333

Email: flavia@ufc.br

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