Tehran University of Medical Sciences Iranian Journal of Allergy, Asthma and Immunology 1735-1502 13 4 2014 08 15 256 264 EN Soodeh Razeghi Jahromi Sina Hospital, Multiple Sclerosis Research Center- Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran AND Shefa Neuroscience Research Center, Tehran, Iran. Seyed Rafi Arrefhosseini Department of Nutrition and Health, Tabriz University of Medical Sciences, Tabriz, Iran. Amir Ghaemi Shefa Neuroscience Research Center, Tehran, Iran AND Infectious Diseases Research Center, Department of Microbiology, Golestan University of Medical Sciences, Gorgan, Iran. Akram Alizadeh Tissue Engineering Department, Advanced Technology in Medicine,Tehran University of Medical Sciences, Tehran, Iran. Hedieh Moradi Tabriz Department of Pathology, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran. Mansoureh Togha Department of Neurology, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran AND Iranian Center of Neurological Research-Neuroscience Institute,Tehran University of Medical Sciences, Tehran, Iran. 2015 10 16 Experimental  allergic encephalomyelitis (EAE) is considered  as the murine model of multiple sclerosis. Daidzein a phytostrogenic compound of soy is known to impose immunomodulatory and antioxidative effects. We conducted this study to assess the potential protective and therapeutic effects of daidzein on allergic encephalomyelitis. C57BL/6 mice  were induced  with  allergic encephalomyelitis  using  myelin oligodendrocyte glycoprotein (35-55) and received daidzein or dimethyl sulfoxide as the vehicle control. To assess the protective effect of daidzein, the mice were administered with 20 mg/kg of daidzein from 21 days prior to 21 days post EAE induction on a daily basis. To evaluate the therapeutic effect of daidzein, mice were fed with 300 mg/kg daidzein after the appearance of the first clinical signs for 10 days. One day after the last gavage, the mice were sacrificed. Spleen and brain were removed for further histological and immunological analysis. Feeding mice with low dose of daidzein prior to disease induction did not affect disease severity. However, treating with high dose of daidzein after the onset of the disease reduced interferon-γ and interleukin-12 secretion, enhanced interleukin-10 production, suppressed lymphocyte proliferation, and decreased cytotoxicity as judged by lactate dehydrogenase release. In conclusion, daidzein reduced the extent of demyelination and disease severity. Chronic oral therapy with low dose of daidzein did not prevent experimental autoimmune encephalomyelitis. However, high doses of daidzein could prohibit disease exacerbation. https://ijaai.tums.ac.ir/index.php/ijaai/article/view/448 https://ijaai.tums.ac.ir/index.php/ijaai/article/download/448/389