Arctigenin regulates Th1 and Th17 differentiation and ameliorates experimental autoimmune encephalomyelitis (THER7P.958)

Abstract

Abstract Arctigenin is a phenylpropanoid dibenzylbutyrolactone lignan extracted from Arctium lappa (L.), and exhibit antitumor, antioxidant and neuron protective activities. But the effects of arctigenin on CNS inflammatory diseases are still unclear. Experimental autoimmune encephalomyelitis (EAE) is an animal model thought to be a T cell-mediated inflammatory demyelination disease. In this study, we in vivo explore the effect of arctigenin on mouse CD4+ effect T helper cell functions. Furthermore, in vitro explore the therapeutic effects and cellular mechanisms of arctigenin on EAE. Arctigenin treated mice are resistant to EAE, the clinical score of arctigenin treated mice is significantly reduced. Histochemistry assay of spinal cord sections also showed that arctigenin reduced inflammation and demyelination in EAE mice. The Th1 and Th17 cells were decreased in the spleens and lymph nodes of arctigenin treated EAE mice, while Th1 cells in CNS did not have significant changes. The expression of Th1 and Th17 cell proliferation and polarizing cytokines are inhibited in arctigenin treated mice spleens and lymph nodes. The Th1 cytokine IFN-γ and transcription factor T-bet, and Th17 cytokines IL-17A, IL-17F, and transcription factor ROR-γt, were significatly suppressed in vitro and in vivo. These suggest that arctigenin have properties of anti-inflammation and immunosuppression, which could be a potential therapeutic drug for multiple sclerosis and other autoimmune inflammatory diseases.