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Introduction: 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. Materials and Methods: 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: 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. Conclusion: 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.

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 Introduction: Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis distinguished by infiltration of leukocytes into the central nervous system. Changes in composition and levels of unsaturated fatty acids, affect the integrity of blood-brain barrier. In this study, we evaluated the effect of Sesame oil on the leukocyte infiltration into the brain of MOG35-55 induced EAE male C57BL/6 mice. Materials and Methods: In this experimental study, male C57BL/6 mice were placed in two therapeutic groups (n=10 per group) with age and weight-matched as follow: 1.Sesame oil-treated EAE mice received 4ml/kg/day of Sesame oil given i.p. from day -3 until day +19 after disease induction, 2.Non-treated EAE mice (EAE control) received Phosphate buffer alone with same schedule. EAE was induced by immunization of mice with MOG35-55 peptide and complete Freund's adjuvant. Leukocytes infiltration into the brain was investigated 20 days after immunization. Data was analyzed using Mann-Whitney U test. Results: The results show that Sesame oil-treated mice had significantly less clinical score of EAE (2.6±0.4) than non-treated EAE induced mice (4.2±0.6), (p<0.001). Also, there was a significant difference at number of the infiltrating cells in brain between Sesame oiltreated (80±20) and non treated EAE-induced mice (150±30), (p<0.01). Conclusion: These results indicate that Sesame oil reduces infiltration of leukocytes into the brain of EAE mice, therefore lessening the histological changes and clinical signs and thus ameliorating the disease.

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Abstract Background: Aloe Vera species have diverse immunomodulatory and antitumor activities. The present study was set out to define the immunomodulatory activity of Aloe Vera extract on tumor necrosis factor-alpha (TNF-α) and development of experimental autoimmune encephalomyelitis (EAE) as an animal model of multiple sclerosis (MS). Materials and Methods: In this experimental interventional study, EAE was induced by MOG35-55 peptide and complete Freund's adjuvant in C57BL/6 mice. Mice were placed in two therapeutic groups (n=8 per group) with the same age and weight. Therapy with Aloe Vera extract (120mg/kg/every day given oral) was started on day 5 before the immunization until 25 day after that. EAE control received phosphate buffer alone with same schedule. Signs of disease were recorded daily until the day 25 when mice were bled and sacrificed. Produced TNF-α by cultured spleen mononuclear cells was detected by ELISA. Results: The Aloe Vera treatment significantly reduced the clinical signs of EAE and delayed onset of disease. Mononuclear cells isolated from spleen of treated-mice with Aloe Vera showed a significant decrease in TNF-α in compared with control mice (p=0.012). Conclusion: Aloe Vera ameliorated the EAE and reduced TNF-α level in MS animal model.