[Effect of vitamin E on the inhibition of experimental autoimmune encephalomyelitis in C57BL/6 mouse]

ABSTRACT

Free radical-mediated per-oxidation of biological molecules, such as lipids, is implicated in the pathogenesis of multiple sclerosis and it's animal model experimental allergic encephalomyelitis [EAE]. Low concentration of antioxidant vitamin E has been observed in serum of multiple sclerosis. However, it is not known whether vitamin E has protective effect in EAE. Vitamin E may inhibit EAE by effect on the level of uric acid and Nitric Oxide [NO] production. In this experimental study some male C57BL/6 mice were placed in two therapeutic groups [n=8 per group] with age and weight-matched as follow 1] Vitamin E-treated EAE mice [10mg/kg/every two days of vitamin E given i.P from day-3 until day + 19 after disease induction, 2] Non-treated EAE mice [EAE control] received vehicle alone with same schedule. In addition, 5 age and weight-matched male C57BL/6 mice served as normal [non-EAE] controls. Clinical score of disease, uric acid and NO levels of the groups were analysed. Results showed that vitamin E-treated mice had significantly less clinical score of EAE [4 +/- 0.8] than non-treated EAE induced mice [5.3 +/- 0.44], [p< 0.01]. Also, there was difference at the onset day of the disease between vitamin E-treated and non-treated EAE-induced mice [day 13 +/- 1 and day 11 +/- 1, respectively], although was not significant. Concentration of uric acid in vitamin E treated mice were significantly lower than EAE control [p< 0.001]. There was no difference at the level of NO between the groups. Vitamin E had no effect on NO level, but decreased serum uric acid level. It suggests that vitamin E can reduce or delay the onset of EAE by increasing uric acid consumption