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Evidence-Based Complementary and Alternative Medicine
Volume 2014, Article ID 345829, 7 pages
http://dx.doi.org/10.1155/2014/345829
Research Article

Effects of Anethole in Nociception Experimental Models

1Department of Pharmacology and Therapeutics, Laboratory of Inflammation, State University of Maringá, Avenida Colombo 5790, 87020-900 Maringá, PR, Brazil
2Department of Pharmacology and Therapeutics, Laboratory of Brain Ischemia and Neuroprotection, State University of Maringá, Maringá, PR, Brazil

Received 26 June 2014; Revised 30 August 2014; Accepted 1 September 2014; Published 25 November 2014

Academic Editor: Jen-Kun Cheng

Copyright © 2014 Alessandra Mileni Versuti Ritter et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

This study investigated the antinociceptive activity of anethole (anethole 1-methoxy-4-benzene (1-propenyl)), major compound of the essential oil of star anise (Illicium verum), in different experimental models of nociception. The animals were pretreated with anethole (62.5, 125, 250, and 500 mg/kg) one hour before the experiments. To eliminate a possible sedative effect of anethole, the open field test was conducted. Anethole (62.5, 125, 250, and 500 mg/kg) showed an antinociceptive effect in the writhing model induced by acetic acid, in the second phase of the formalin test (125 and 250 mg/kg) in the test of glutamate (62.5, 125, and 250 mg/kg), and expresses pain induced by ACF (250 mg/kg). In contrast, anethole was not able to increase the latency time on the hot plate and decrease the number of flinches during the initial phase of the formalin test in any of the doses tested. It was also demonstrated that anethole has no association with sedative effects. Therefore, these data showed that anethole, at all used doses, has no sedative effect and has an antinociceptive effect. This effect may be due to a decrease in the production/release of inflammatory mediators.