Therapeutic Effect of EDTA in Experimental Model of Multiple Sclerosis

Abstract

Multiple sclerosis (MS) is a chronic, neurodegenerative disease that causes central nervous system (CNS) demyelination and affects approximately 2 million people worldwide. The aim of the present study was to test the therapeutic effect of ethylene diamine tetra acetic acid (EDTA) in an experimental model of MS. The experiment was done on male C57BL/6 mice aged 6–8 weeks. The experimental autoimmune encephalomyelitis (EAE) was induced using 250 μg of the MOG35-55 peptide emulsified in CFA and injected subcutaneously on day 0 over two flank areas. In addition, 250 ng of pertussis toxin in 400 μl PBS was injected i.p. on days 0 and 2. In the treatment group, EDTA was administered i.p. at a dose 75 mg/kg/day. The mice were sacrificed 21 days after EAE induction and blood samples were taken from their hearts. The brains of mice were removed for histological analysis and their isolated splenocytes were cultured. Results: Our results showed that treatment with EDTA caused a significant delay in the time of onset and a significant reduction in severity of the EAE. Histological analysis indicated that there was not any plaque in the group of EDTA-treated mice whereas 5 ± 1 plaques were detected in controls. The density of mononuclear infiltration in the CNS of EDTA-treated mice was lower than controls. In the group of EDTA-treated mice, using the FRAP test, total serum antioxidant power was high and significant in comparison to the controls. Moreover, the serum level of nitric oxide in the treatment group was significantly less than the control group, and, also, the levels of IFN-γ in the cell culture supernatant of treated mice splenocytes was lower than control group. These data indicate that EDTA therapy can effectively attenuate EAE progression.

Keywords::

• MS
• EAE
• EDTA
• multiple sclerosis
• chelation therapy the

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.