Multiple sclerosis (MS) is a chronic neurologic disease defined by inflammation and demyelination of the central nervous system (CNS) comes with variable degrees of axonal and neuronal damage. The efficacy of β-D-Mannuronic acid (M2000) as a novel drug with immunosuppressive properties, patented (PCT/EP2017/067920), has been shown in experimental model of MS. In this study, the effects of M2000 on IL-1β, IL-17A, STAT1 and STAT3 gene expression and TLR2 and TLR4 molecules in secondary progressive MS (SPMS) patients have been evaluated. In this study, 14 SPMS patients and 14 healthy subjects (as control group) were entered from the phase 2 clinical trial (Clinical Trial identifier, IRCT2016111313739N6). The gene expression of IL-1β, IL-17A, STAT1 and STAT3 was assessed at the baseline and then measured after 6 months of therapy with M2000, by using quantitative real-time PCR method. Moreover, the expression of TLR2 and TLR4 molecules on peripheral blood mononuclear cell (PBMCs) were evaluated by flow cytometry method. The gene expression of IL-17A, STAT1 and STAT3 in MS patients decreased after six months of therapy with M2000 comparing before treatment. Also, the gene expression of IL-1β, decreased numerically after six months. Furthermore, the expression of TLR2 and TLR4 on PBMCs of the patients declined when compared to baseline. The results of this investigation revealed that M2000 could downregulate IL-17, STAT1 and STAT3 genes in SPMS patients and also reduce the expression of TLR2 and TLR4 on PBMCs. Moreover, M2000 declined numerically IL-β gene expression.

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