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Evidence-Based Complementary and Alternative Medicine
Volume 2012, Article ID 918174, 9 pages
http://dx.doi.org/10.1155/2012/918174
Research Article

Copaiba Oil-Resin Treatment Is Neuroprotective and Reduces Neutrophil Recruitment and Microglia Activation after Motor Cortex Excitotoxic Injury

1Laboratory of Experimental Neuroprotection and Neuroregeneration, Institute of Biological Sciences, Federal University of Pará, 66075-900 Belém, PA, Brazil
2Brain Institute, Federal University of Rio Grande do Norte, Natal, RN, Brazil
3Laboratory of Ore Processing, Federal University of Pará, Marabá, PA, Brazil
4Chemistry Laboratory, Federal University of Pará, Abaetuba, PA, Brazil
5Laboratory of Biotechnology, EMBRAPA, Belém, PA, Brazil

Received 23 September 2011; Revised 5 November 2011; Accepted 16 November 2011

Academic Editor: Bhushan Patwardhan

Copyright © 2012 Adriano Guimarães-Santos 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

The oil-resin of Copaifera reticulata Ducke is used in the Brazilian folk medicine as an anti-inflammatory and healing agent. However, there are no investigations on the possible anti-inflammatory and neuroprotective roles of copaiba oil-resin (COR) after neural disorders. We have investigated the anti-inflammatory and neuroprotective effects of COR following an acute damage to the motor cortex of adult rats. Animals were injected with the neurotoxin N-Methyl-D-Aspartate (NMDA) ( ) and treated with a single dose of COR (400 mg/kg, i.p.) soon after surgery (Group 1) or with two daily doses (200 mg/kg, i.p.) during 3 days (Group 2) alter injury. Control animals were treated with vehicle only. COR treatment induced tissue preservation and decreased the recruitment of neutrophils and microglial activation in the injury site compared to vehicle animals. The results suggest that COR treatment induces neuroprotection by modulating inflammatory response following an acute damage to the central nervous system.