Riboflavin supplementation improves neurological disability but not spatial cognition mediated with increased gene expression and protein levels of BDNF in the brain and spinal cord in murine model of multiple sclerosis

International Congress on Neuroimmunology and Therapeutics

DoubleTree by Hilton Hotel San Francisco Airport, San Francisco, CA, USA

Mahshid Naghashpour1, Reza Amani1, Alireza Sarkaki1, Ata allah Ghadiri1, Alireza Samarbafzadeh1 and Ahmad Rouhizadeh1,2

Posters-Accepted Abstracts: J Neurol Disord

Abstract :

Introduction: Interferon beta-1A (IFNβ-1A) is the major treatment for MS. However, this treatment is not always effective. It has been showed that riboflavin is important in the myelin formation. The interactions between potential effects of riboflavin and IFNβ-1A on neurological disability, learning and memory as well as the gene expression and protein levels of brain-derived neurotrophic factor (BDNF) in the brain and spinal cord of experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS) were evaluated. Methods: Fifty-six female C57BL/6 mice at +10 weeks of age underwent EAE induction. Riboflavin at 10 mg/Kg of body weight and/or IFNβ-1A at 150 IU/g of body weight were administrated for two weeks. The mice (n=56) were assigned into7 groups randomly (with 8 in each): sham operated 1 [SO1], PBS; sham operated 2 [SO2], PBS+riboflavin; sham treatment 1 [ST1], EAE+same volume of water (as vehicle of riboflavin); sham treatment 2 [ST2] EAE+sodium acetate buffer (as vehicle of IFNβ-1A); treatment 1 [T1], EAE+IFNβ-1A; treatment 2 [T2], EAE+riboflavin; treatment 3 [T3], EAE+IFNβ-1A+riboflavin. mRNA was quantitated for BDNF using Real-time PCR system. Levels of the BDNF were quantified using the BDNF EMAX® ImmunoAssay System. Spatial learning and memory were assessed using the standard Morris water maze (MWM). Results: Treatment the EAE mice with combination of the riboflavin and IFNβ-1A improved neurological disability significantly (P<0.01) by increasing the gene expression and BDNF level in both brain and spinal cord of EAE mice. T2 Mice treated with riboflavin swam significantly faster than ST2 and T1 mice. T3 mice treated with both riboflavin and INFβ-1A swam significantly faster than ST1 mice on day 4 of the trial (P=0.003). Conclusion: Our findings address the therapeutic effects of riboflavin and highlight the synergistic role of riboflavin with IFN- β1A on neurological disability improvement probably mediated by BDNF levels in the brain and spinal cord in an experimental model of MS.