Abstract

Context: The immune system through T-helper 1 (Th1) and Th17 cells play a critical role in the pathogenesis of experimental autoimmune encephalomyelitis (EAE), whereas the Th2 responses inhibit myelin degeneration. Artemisinin, as an anti-malaria as its agent, has been used widely in the treatment of malaria, shifts the lymphocyte responses from Th1 to Th2.Objective: In this study, we have investigated the therapeutic effects of artemisinin on the EAE treatment.Materials and methods: EAE was induced in the inbred C57BL6 mice. High and low doses of prednisolone and artemisinin were injected daily with the control and test groups, respectively. The spleen and the brain of the mice were removed and used for ELISA and histological studies.Results: The mean weight of mice was significantly (p value < .05) higher in artemisinin-treated group compared with the untreated group, whereas, the mean EAE score of mice was significantly (p value < .05) lower in the artemisinin-treated group compared with the untreated group. The brain histology shows the absence of plaque formation in the artemisinin treated group. The concentration of IFN-γ in the low dose of artemisinin treated group showed significantly (p value < .05) lower in comparison to the untreated group. IL-4 concentration was significantly (p value < .05) higher in the treated groups than the control group.Conclusions: Since, artemisinin can shift the immune responses from Th1 to Th2, therefore, it can be helpful in the treatment of MS after more investigation.

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