Abstract
Experimental autoimmune encephalomyelitis (EAE) is a murine autoimmune disease used to study multiple sclerosis. We have investigated the 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 H2O2, NO, IFN-γ TNF-α and IL-17 production spontaneously or after ConA and MOG35–55 stimulation. 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.
Highlights
Multiple sclerosis (MS) is an autoimmune inflammatory and chronic disease of the central nervous system (CNS) characterized by multifocal demyelinating lesions in the white matter, gliosis and subsequent diffuse axonal damage, which results in a progressive neurological function deficit [1]
Copaiba oil has been reported to reduce neutrophil recruitment and microglia activation, as well as to induce neuroprotection in the CNS by modulating an acute inflammatory response [6]. These findings suggest that copaiba oil may inhibit inflammatory responses involved in both MS and EAE
Copaiba oil has never been evaluated in inflammatory mediators involved in EAE and most of studies on copaiba oil are related to its chemical composition, the aim of this study was to evaluate the immunomodulatory effects of copaiba oil on H2O2, nitric oxide (NO), IFN-γ, TNF-α and IL-17 production in culture of splenocytes from C57Bl/6 mice induced with EAE
Summary
Multiple sclerosis (MS) is an autoimmune inflammatory and chronic disease of the central nervous system (CNS) characterized by multifocal demyelinating lesions in the white matter, gliosis and subsequent diffuse axonal damage, which results in a progressive neurological function deficit [1]. The development of more effective drugs would be of great clinical benefit in the treatment of MS. 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. New therapies for the treatment of MS are focused on drugs that are able to modulate the production of inflammatory mediators [4,5,6]
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