Planta Med 2014; 80 - P1C9
DOI: 10.1055/s-0034-1394634

Effects of licochalcone A on immunomodulation in a murine model of multiple sclerosis

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.
  • 2Laboratory of Experimental Immunology and Pathology, CBR, Federal University of Juiz de Fora, Juiz de Fora

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.

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, Licochalcone A, Experimental autoimmune encephalomyelitis, cytokines.


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.

4. Funakoshi-Tago et al (2008) Biochem Pharmacol 76, 1681 – 1693