Immunomodulatory effects of licochalcone A on experimental autoimmune encephalomyelitis

Experimental autoimmune encephalomyelitis (EAE) is a murine autoimmune disease used to study multiple sclerosis. Herein, we have investigated the immunomodulatory effect of licochalcone A (LicoA) on NO, H2 O2 , tumour necrosis factor-alpha (TNF-α), interferon gamma (IFN-γ) and IL-17 production in cultured cells from EAE mice.

EAE was induced in C57Bl/6 mice with myelin oligodendrocyte glycoprotein peptide (MOG35-55 ). LicoA was isolated from the roots of Glycyrrhiza inflata. Splenocytes were obtained from EAE mice and incubated with LicoA (4, 20 and 40 μm). Peritoneal cells were obtained from EAE mice treated with LicoA (15 and 30 mg/kg/day. p.o.). H2 O2 , NO, IFN-γ, TNF-α and IL-17 production was determined in the presence or absence of concanavalin (ConA) or MOG35-55 stimulation.

LicoA (40 μm) inhibited H2 O2 , NO, IFN-γ, TNF-α and IL-17 production in splenocytes spontaneously or after both ConA and MOG35-55 stimulation. LicoA (30 mg/kg/day) reduced clinical score and severity of EAE mice, and inhibited TNF-α, IFN-γ and IL-17 production in peritoneal cells.

LicoA possesses immunomodulatory effects on H2 O2 , NO, IFN-γ, TNF-α and IL-17 production in cells from EAE mice. 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.