Multiple sclerosis (MS) is a chronic inflammatory
demyelinating disease leading to axonal injury. Even if the etiology of MS is still unknown the disease begins with
inflammation involving autoreactive T lymphocytes activation in genetically susceptible subjects.
Interferon beta-1b (IFN β 1b) is one of the most used drug in the MS
therapy. The results obtained in this study show that the concentration of SOD1 in CSF of relapsing-remitting MS (RR-MS) patients, evaluated by
enzyme-linked
immunosorbent assay (ELISA), is decreased compared to pathological controls. Moreover, the Western blotting analysis demonstrated that SOD1 in human peripheral blood mononuclear cells (PBMC) in healthy controls was significantly higher compared to MS subjects before starting DMT
therapy. In addition IFN β 1b
therapy causes an increase of intracellular
SOD1 protein as well as
mRNA levels in PBMC. Moreover, the treatment of
neuroblastoma SK-N-BE cells with IFN β 1b increased
SOD1 protein and
mRNA levels; these data also suggest that
neuroprotective effect of this physiological molecule is, at least in part, carried out through its effect on SOD1. This study demonstrate that DMT
therapy is able to increase SOD1 expression in PBMC of RR-MS patients. Therefore, the effectiveness of DMT
therapy can be ascribed, at least in part, to an increased levels of this
antioxidant enzyme as further confirmed by in vitro studies in SK-N-BE cells.