Fig. 7

Long-term protective effects of apocynin after EAE induction. Clinical disease scores were recorded daily until 45 days after induction. The clinical signs of EAE first appeared on day 14 and reached peak levels on day 20 from the 1st MOG (M) immunization. Apocynin (EAE + apocynin, n = 6) or its vehicle (EAE + vehicle, n = 6) was orally administered during the entire period. Control groups also received oral Apocynin (sham + apocynin, n = 2) or vehicle only (sham + vehicle, n = 2) without (N) MOG immunization. a Apocynin profoundly reduced the EAE clinical score induced by MOG. Data are mean ± sem (n = 2–6). *p < 0.05 compared with apocynin-treated group. General linear models verified statistical significant differences in clinical scores by time and treatment and interaction between time and treatment was also noticed. b Apocynin did not influence the rate of EAE induction by MOG. 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 of the left-hand panel was enlarged two times and illustrated in the right-hand panel. Scale bar represents 50 μm