Abstract
Silybin, a peculiar flavonoid compound derived from the fruit and seeds of Silybum marianum, exhibits strong anti-inflammatory activities. In the present study, we found that silybin effectively alleviated experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), via inhibition of dendritic cell (DC) activation and Th17 cell differentiation. Silybin treatment greatly ameliorated the disease severity and significantly declined inflammation and demyelination of the central nervous system (CNS) of EAE mice. Consistent with the disease development, silybin-treated bone marrow-derived DCs (BM-DCs) exhibited reduced costimulatory molecules (e.g., CD80 and CD86) and MHC II expression. These results demonstrated the distinguished bioactivity of silybin for suppressing DC activation, inhibiting pathogenic Th17 inflammatory cell responses, and, eventually, alleviating EAE severity. Taken together, our results show that silybin has high potential for the development of a novel therapeutic agent for the treatment of autoimmune diseases such as MS.
Highlights
Multiple sclerosis (MS) is an inflammatory and neurodegenerative demyelinating disease of the central nervous system (CNS)
We noticed that silybin at 10 and 20 mg/kg/day is optimal for alleviating EAE development (p < 0.05; Figures 1A,B)
To dissect the ability of silybin in EAE, treatment began on day 10 p.i., when pathogenic T cells had begun migrating to the CNS [16]
Summary
Multiple sclerosis (MS) is an inflammatory and neurodegenerative demyelinating disease of the central nervous system (CNS). The definite pathogenesis has not been illuminated clearly, increasing evidences endorse that MS is an autoimmune disease with irreversible white matter (WM) damage [2, 3]. At the early phase of EAE, myelin-specified CD4+ T cells, as well as dendritic cells (DCs), B cells, and macrophages, are triggered in the periphery and penetrated the CNS. Among diverse CD4+ T-cell subsets, interleukin-17 (IL-17)-positive Th17 cells, which secrete IL-17A, are regarded as the primary effector cells in provoking an inflammatory response in MS/EAE [4]. Antigen-presenting cells (APCs) exert an essential function in MS/EAE by activating naïve T cells, among which DCs are experts at regulating rest T-cell polarization with antigen peptides present [5]
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