alexa Brain-derived Neurotrophic And Immunologic Factors: Beneficial Effects Of Riboflavin On Motor Disability In Murine Model Of Multiple Sclerosis
ISSN: 2329-6895

Journal of Neurological Disorders
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2nd International Conference on Neuroimmunology & Therapeutics
December 01-02, 2016 Atlanta, USA

Mahshid Naghashpour
Ahvaz Jundishapur University of Medical Sciences, Iran
Posters & Accepted Abstracts: J Neurol Disord
DOI: 10.4172/2329-6895.C1.015
Abstract
In the present study, C57BL/6 female mice (n=56) were used to explore the neuroprotective effects of riboflavin in motor disability of experimental autoimmune encephalomyelitis (EAE) as a model of multiple sclerosis. The animals were assigned into 7 groups: Sham operated 1 (SO1), healthy mice received PBS (Phosphate Buffer Saline); Sham operated 2 (SO2), healthy mice received PBS and riboflavin; Sham treatment 1 (ST1), EAE mice received water; Sham treatment 2 (ST2), EAE mice received sodium acetate buffer; Treatment 1 (T1), EAE mice received interferon beta-1a (INFβ-1a); Treatment 2 (T2), EAE mice received riboflavin; Treatment 3 (T3), EAE mice received INFβ-1a and riboflavin. After EAE induction, scoring was performed based on clinical signs. By detecting score 0.5, riboflavin at 10 mg/kg of body weight and/or INFβ-1a at 150 IU/g of body weight administration were started for two weeks. The brain and spinal cord levels of brain-derived neurotrophic factor (BDNF), interleukin-6 (IL-6), and interleukin-17A (IL-17A) were studied using real-time PCR and ELISA methods. BDNF expression and protein levels were increased in the brain and spinal cord of the T3 group compared with the other groups (P<0.01). IL-6 and IL-17A expression were increased in the brains of the T3 and T1, respectively, compared to the other groups (P<0.01). Daily clinical score was reduced significantly by riboflavin in both effector and chronic phases of the disease compared with that of controls (p<0.05). Our findings showed that riboflavin is capable for suppressing the neurological disability mediated by BDNF and IL-6.
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