Planta Med 2014; 80 - P1C26
DOI: 10.1055/s-0034-1394651

Copaiba oil suppress inflammatory cytokines in splenocytes of C57Bl/6 mice induced with experimental autoimmune encephalomyelitis (EAE)

D dos Santos Dias 1, LB Almeida Fontes 1, 3, AE Miller Crotti 2, BJV Aarestrup 3, FM Aarestrup 3, AA Da Silva Filho 1, 3, JO do Amaral Corrêa 1, 3
  • 1Department of Pharmaceutical Sciences, Faculty of Pharmacy, Federal University of Juiz de Fora, Juiz de Fora
  • 2Department of Chemistry, Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto, University of São Paulo
  • 3Laboratory of Experimental Immunology and Pathology, CBR, Federal University of Juiz de Fora

Multiple sclerosis (MS) is an autoimmune inflammatory and chronic disease of the central nervous system [1]. The experimental autoimmune encephalomyelitis (EAE) is an appropriate model for the study of the underlying pathogenesis of MS, since it resembles MS in its clinical, histopathological, and immunological features. It is known that the immunopathogenesis of both EAE and MS is immune-mediated mainly by Th1 and Th17 cells, while both cells (Th1 and Th17) induce the production of oxygen radicals, such as nitric oxide (NO) and hydrogen peroxide (H2O2) [2]. However, treatment of MS is expensive and possess limited efficacy [2]. Copaiba oil, which is obtained from several species of Copaifera L. (Leguminosae), is popularly known as “copaiba”. Copaiba oil has been used in Brazil, especially in Amazonas state, as anti-inflammatory [3]. Also, studies have demonstrated that copaiba oil can ameliorate the outcome of some inflammatory-mediated diseases. These findings suggest that copaiba oil may also inhibit inflammatory responses involved in both MS and EAE. Then, we have investigated the in vitro immunomodulatory effects of copaiba oil (100, 50 and 25 µg/mL) on NO, H2O2, TNF-α, IFN-γ and IL-17 production in cultured cells from EAE-mice. Copaiba oil (100 µg/mL) inhibited significantly H2O2, NO, IFN-γ, TNF-α and IL-17 production spontaneously or after ConA and MOG35 – 55 stimulation in comparison with EAE group. GC-MS analysis of copaiba oil showed as major compound β-caryophyllene. It is suggested that copaiba oil acts on the mechanism of development of EAE by IFN-γ, IL-17 and TNF-α inhibition, modulating the immune response on both Th1 and Th17 cells mainly due to the presence of β-caryophyllene, which presents immunosuppressive effects and may limit the inflammatory response.

Acknowledgements: This work was supported by grants from FAPEMIG (CBBAPQ 04257/10; APQ 00171/11). We are thankful to PIBIC/CNPq/UFJF, CNPQ and CAPES for fellowships and scholarships.

Keywords: Multiple sclerosis, Copaiba oil, β-caryophyllene.


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