Effect of Sesame oil on leukocyte infiltration into the brain of C57/BL6 mice with experimental autoimmune encephalomyelitis

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 MOG[35-55] induced EAE male C57BL/6 mice. 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 MOG[35-55] 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. 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 oil-treated [80 +/- 20] and non treated EAE-induced mice [150 +/- 30], [p<0.01]. 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

Effect of simvastatin on evolution of experimental autoimmune encephalomyelitis in C57BL/6 mice

Simvastatin is an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme a reductase and widely used as cholesterol-lowering agent. It is a promising candidate for future treatment in multiple sclerosis [MS], as it has been shown to exhibit immunomodulatory and anti-inflammatory effects. This study examined the effect of simvastatin on the evolution of experimental autoimmune encephalomyelitis [EAE], as an animal model for MS. EAE was induced by immunization of 8 week old C57BL/6 mice with MOG35-55 peptide with complete Freunds adjuvant. Therapy with simvastatin [1mg/kg/every day given as oral] was started on day 3 before the immunization until 25 day after immunization Total antioxidant capacity [TAC] was assessed by ferric reducing-antioxidant power [FRAP] method. Nitric oxide [NO] production was also estimated by Griess reaction. The results show that simvastatin-treated mice had significantly less incidence and clinical score of EAE than non-treated [control] EAE induced mice [p=0.001 and p=0.0001, respectively]. Moreover, treated mice displayed a significantly delayed disease onset compared with control mice. Simvastatin significantly increased TAC and level serum uric acid [p=0.001], but had no effect on serum nitrite production. Our results suggest that simvastatin therapy may be effective in the prevention of symptomatic EAE. This resistance to encephalomyelitis may be associated with the inhibition of oxidative stress and the increase of antioxidant capacity

[Effect of vitamin D3 on IFN-T and IL-10 levels in mice with experimental a utoimmune encephalomylitis]

Multiple sclerosis [MS] is a chronic autoimmune disease with unknown etiology affecting the central nervous system. The pre9alence of MS is highest where environmental supplies of vitamin Dare lowest. Some studies have shown a strong protective effect of vitamin D3 in experimental autoimmune encephalomyelitis [EAE]; a model of MS. However, it is not known whether vitamin D3 has a protective effect in EAE. Vitamin D3 may be inhibit EAE by having an effect on TH1 and TH2 immune responses. To address this question, the effect of vitamin D[3] on cellular immune responses in C57BL/6 mice with experimental autoimmune encephalomyelitis was investigated. Male C57HL/6 mice matched in age and weight were placed in two therapeutic groups [n10 per group] as follows: Vitamin D3-treated EAE mice [5 micro g/kg/every two days of vitamin D3 given i.p from day -3 until day +19 after disease induction]. Non-treated EAE mice [EAE control] received vehicle alone with same schedule. 20 days after immunization, the mononuclear cells [MNCs] of the spleen were isolated from mice and cultured in the presence and absence of MOG35-55 for 96 hours. The supematant of cultured cells was collected and produced cytokines [IL-10 and IFN-gamma] were assayed by ELISA. The results showed that vitamin D3-treated mice had less severe clinical signs and synptoms of EAE [3.2 +/- 0.8] than non-treated EAE induced mice [5.3 +/- 0.44]. [p=0.001]. Also, there was a significant difference regarding the day of onset of disease in the vitamin D3-treated and non treated EAE-induced mice [day 15 +/- 1 and day 11 +/- 1, respectively]. There was no significant difference in IFN-y production between treated and non-treated mice, but the amount of 11-10 production in the D3-treated mice was higher than the non-treated group [p=0.001]. Considering the role of TH1 in the pathogenesis of EAE and MS. it is suggested that vitamin D3 can reduce or delay the onset of EAE by shifting immune responses to TH2 and IL-10 production. Thus, vitamin D3 as an immune modulatory agent is potentially important for treatment of MS

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

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