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

Free radical-mediated peroxidation 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.