Oxidative stress activity of fingolimod in multiple sclerosis

Abstract

ObjectiveMultiple sclerosis (MS) is a demyelinating chronic inflammatory disease of the central nervous system (CNS). Recent studies have shown that oxidative stress plays an important role in MS pathogenesis. This study aimed to investigate the relationship between total oxidative stress (TOS) and total antioxidant capacity (TAC), which were reported to be effective in the pathogenesis of MS, and therapeutic efficacy of fingolimod used in the treatment of MS. Materials and methodsSerum TOS and total TAC levels of 25 patients with relapsing-remitting MS (RRMS) were measured before fingolimod treatment was initiated and in the third month of treatment and compared with those of 40 healthy individuals. Measurement of TOS activity was performed with TOS Assay Kit (Rel Assay Diagnostics, Turkey). Measurement of TAC activity was also performed with TAC Assay Kit (Rel Assay Diagnostics, Turkey). ResultsA statistically significant increase was observed in the TOS levels measured before fingolimod treatment in the patient group compared to the control group. The TOS levels measured in the third month of the treatment were found to decrease significantly compared to the pre-treatment TOS levels. An increase was observed in TAC levels after the treatment; however, no significant difference was found between the groups in terms of TAC levels. There was a positive correlation between the pre- and post-treatment Expanded Disability Status Scale (EDSS) scores and TOS values whereas no significant correlation was observed between the pre- and post-treatment EDSS scores and TAC values. ConclusionThe present study has revealed that fingolimod reduced oxidative stress. There was a positive correlation between the pre- and post-treatment EDSS and TOS values, which confirmed that there was a close correlation between the MS and oxidative stress. There are some limitations in this study. The small number of patients and the short follow-up times can be listed among these limitations. Our study does not contain a definitive answer to what is the mechanism of increased TOS in MS patients and how fingolimod reduces TOS levels. More detailed studies are needed on this subject.