Multiple sclerosis (MS) is the most common chronic inflammatory disease of the central nervous system (CNS) characterized by aberrant auto reactive T cell responses, combined with dysfunction of the regulatory network of the immune system [1,2]. Experimental autoimmune encephalomyelitis (EAE) is a commonly accepted animal model for MS and can be induced in susceptible rodents and other animals by immunization with myelin antigens, such as myelin oligodendrocyte glycoprotein (MOG). In MS and EAE, the response is mediated by autoimmune Th1 and Th17 cells and the production of multiple proinflammatory cytokines/chemokines and other inflammatory mediators, including INF-γ, TNF-α and IL-17. As a result, new therapies for MS treatment are focused on compounds that are able to modulate the production of inflammatory mediators. Licochalcone A (LicoA), a natural chalcone obtained mainly from roots of Glycyrrhiza species, is able to inhibit inflammatory mediators present in the immunopathogenesis of both MS and EAE [3,4]. Then, we have investigated the in vivo immunomodulatory effects of LicoA induced in C57Bl/6 mice with MOG35 – 55. LicoA was isolated from the roots of G. inflata and peritoneal cells were obtained from EAE-mice treated with LicoA (15 and 30 mg/kg/day. p.o.). IFN-γ, TNF-α and IL-17 production was determined in the presence or absence of concavalin A (ConA) and/or MOG35 – 55 stimulation. LicoA (30 mg/kg/day) reduced the clinical score and the severity of EAE-mice. Also, LicoA (30 mg/kg/day) inhibited TNF-α, IFN-γ and IL-17 production in peritoneal cells. Based on results, it is suggested that LicoA acts on the mechanism of development of EAE by inhibition of IFN-γ, IL-17 and TNF-α, modulating the immune response on both Th1 and Th17 cells.

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.

Experimental autoimmune encephalomyelitis (EAE) is a murine autoimmune disease used to study multiple sclerosis. Multiple sclerosis (MS) is an autoimmune inflammatory and chronic disease of the central nervous system. 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) [1,2]. As a result, new therapies for MS treatment are focused on compounds that are able to modulate the production of inflammatory mediators [1,2]. Among natural compounds with possible therapeutic applications on MS, is licochalcone A (LicoA), which is obtained from roots of Glycyrrhiza species, mainly G. inflata (Fabaceae). Studies have demonstrated that LicoA is able to inhibit inflammatory mediators present in the immunopathogenesis of both MS and EAE [3].Then, we have investigated the in vitro immunomodulatory effects of LicoA induced in C57Bl/6 mice with MOG35 – 55. LicoA was isolated from the roots of G. inflata and splenocytes were obtained from EAE mice and incubated with LicoA (4, 20 and 40µM). LicoA (40µM) 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. It is suggested that LicoA 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. Considering LicoA as a promising compound for the treatment of inflammatory and demyelinating diseases, such as MS, further studies are in progress to disclose its in vivo effects on EAE model.