Planta Med 2014; 80 - P1C14
DOI: 10.1055/s-0034-1394639

In vitro evaluation of the immunomodulatory effects of Licochalcone A on Experimental Autoimmune Encephalomyelitis (EAE)

LB Almeida Fontes 1, 2, BJV Aarestrup 2, FM Aarestrup 2, AA Da Silva Filho 1, 2, JO do Amaral Corrêa 1, 2
  • 1Department of Pharmaceutical Sciences, Faculty of Pharmacy, Federal University of Juiz de Fora, Brazil
  • 2Laboratory of Experimental Immunology and Pathology, CBR, Federal University of Juiz de Fora, Brazil

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.

Acknowledgements: This work was supported by grants from the Fundação de Apoio a Pesquisa do Estado de Minas Gerais (FAPEMIG, CBBAPQ 04257/10 and APQ 00171/11). We are thankful to PIBIC/CNPq/UFJF, CNPQ and CAPES for fellowships and scholarships.

Keywords: Experimental autoimmune encephalomyelitis, licochalcone A, Multiple sclerosis, immune response


1. Fontes, LBA et al. (2014)J Pharm Pharmacol, 66, 886 – 894.

2. Correa, JOA et al. (2010) Exp Neurol, 226, 15 – 23.

3. Furusawa JI et al (2009) Cell Signal, 21, 778 – 785.