Abstract
Multiple sclerosis (MS) is an autoimmune inflammatory disease. Inflammatory infiltrates and demyelination of the CNS are the major characteristics of MS and its related animal model-experimental autoimmune encephalomyelitis (EAE). Immoderate autoimmune responses of Th17 cells and dysfunction of Treg cells critically contribute to the pathogenesis of MS and EAE. Our previous study showed that Ginsenoside Rd effectively ameliorated the clinical severity in EAE mice, but the mechanism remains unclear. In this study, we investigated the therapeutic effect of Ginsenoside Rd on EAE in vivo and in vitro and also explored the potential mechanisms for alleviating the injury of EAE. The results indicated that Ginsenoside Rd was effective for the treatment of EAE in mice and splenocytes. Ginsenoside Rd treatment on EAE mice ameliorated the severity of EAE and attenuated the characteristic signs of disease. Ginsenoside Rd displayed the therapeutic function to EAE by modulating inflammation and autoimmunity, via the downregulation of related proinflammatory cytokines IL-6 and IL-17, upregulation of inhibitory cytokines TGF-β and IL-10, and modulation of Treg/Th17 imbalance. And the Foxp3/RORγt/JAK2/STAT3 signaling was found to be associated with this protective function. In addition, analysis of gut microbiota showed that Ginsenoside Rd also had modulation potential on gut microbiota in EAE mice. Based on this study, we hypothesize that Ginsenoside Rd could be a potential and promising agent for the treatment of MS.
Highlights
Multiple sclerosis (MS) is an autoimmune inflammatory disease affecting the central nervous system (CNS) of the body [1]
As the above results suggested that Ginsenoside Rd could regulate the inflammation and Treg/T helper 17 (Th17) cell imbalance in splenocytes with EAE, we further investigated the effect of Ginsenoside Rd on the Foxp3/RORγt/JAK2/STAT3 signaling pathway
Ginsenoside Rd treatment of EAE ameliorated the severity of EAE and attenuated the characteristic signs of disease
Summary
Multiple sclerosis (MS) is an autoimmune inflammatory disease affecting the central nervous system (CNS) of the body [1]. CD4+ T cells regulated autoimmune/inflammatory response is thought to critically associate with this disease. T cells enter into the CNS through the damaged blood-brain barrier (BBR), initiate a series chain-type inflammatory response, to induce inflammation, demyelization, oligodendrocyte loss, and subsequent axonal and neuronal damage [3]. For the study of MS, rat experimental autoimmune encephalomyelitis (EAE) is the most widely used animal model. While it is not a so perfect set of animal model, it can mimic mainly pathological features of MS and can be used for pathophysiology and therapy study [6]
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