فهرست مطالب a. ebrahim habibi

In the present study, we examined the possibility of astaxanthin usage in the MS model of mice, experimental autoimmune encephalomyelitis (EAE). EAE disease was induced using MOG35-55 peptide and complete Freund adjuvant (CFU) in female C57BL/6 mice. Mice were divided into control, patient group (MS model, EAE), and prevention group, the group received astaxanthin for 21days before immunization, and astaxanthin treatment was initiated when mice showed the first symptoms of EAE. Each group consisted of 8 mice. The consumption of Astraxanthin was continued for 35 days, and each mouse received astaxanthin about 0.4% of the weight of used pellet (about 400 mg). Cell proliferation was measured by MTT, IL1β, but IL6 levels (proinflammatory cytokines) were measured by ELISA. In addition, the spinal cord tissues were also taken for immunohistopathological evaluations. Based on the results, the use of astaxanthin produced appropriate clinical and pathological outcomes, lead to decrement of IL1β, and IL6 proinflammatory cytokines (P<0.0001) production. Immunohistopathologic studies also showed a decrease in leukocyte infiltration in the spinal cord of experimental groups. Overall, this drug approach can be considered as a useful strategy in the prevention and treatment of multiple sclerosis.