Fig. 1

Apocynin ameliorates the clinical signs and disease progression of MOG-induced EAE. Clinical disease scores were recorded daily until 21 days after induction. The clinical signs of EAE first appeared on day 11 and reached peak levels on day 19 from the 1st MOG (M) immunization. Apocynin (EAE + apocynin, n = 12) or its vehicle (EAE + vehicle, n = 12) was orally administered during the entire period. Control groups also received oral apocynin (sham + apocynin, n = 6) or vehicle only (sham + vehicle, n = 7) without (N) MOG immunization. a Apocynin profoundly reduced the EAE clinical score induced by MOG. Data are mean ± sem (n = 6–12). *p < 0.05 compared with apocynin-treated group. General linear models verified statistically significant differences in clinical scores by time and treatment, and interaction between time and treatment was also noticed. b Apocynin reduced the incidence rate of EAE induced by MOG. c, d Apocynin reduced MOG-induced demyelination in spinal cord of EAE mice. Mice were sacrificed 3 weeks after MOG injection, and sections of spinal cord were evaluated for damaged myelin sheaths using luxol fast blue (LFB). The presence of white matter lesions are reflected by reduced LFB staining in the spinal cord. c LFB staining of the spinal cord shows extensive demyelination in the MOG-immunized EAE mice. EAE-associated demyelination is almost completely absent in EAE mice treated with apocynin. The square area in the low magnification view seen in the left-hand panel was enlarged four hundred times and illustrated in the right-hand panel. Scale bar represents 50 μm. d The graph represents percent of demyelination of white matter of the thoracic spinal cord with or without apocynin treatment in EAE mice. Data are mean ± sem (n = 3). *p < 0.05 compared with the apocynin-treated group