Fig. 11

Reduced astrocyte and microglia reactivity and lymphocyte infiltration in the nimodipine-treated spinal cord. A Representative coronal sections of lumbar spinal cords immunostained for GFAP, Iba1, and CD45. Tissue was collected from untreated subjects and EAE mice treated with vehicle or nimodipine during the acute and peak phase of the disease. Scale bar, 90 μm. B qPCR analysis of TGFβ, IFNγ, IL1β, IL6, and IL10 in spinal cord samples from untreated subjects and EAE mice treated with vehicle or nimodipine during the acute and peak phase of the disease. GAPDH and TBP were used as internal standards and values are expressed as fold change of untreated values ± SEM. C Density of GFAP-positive cells and integrated fluorescence intensity of Iba1 and CD45 were quantified in the entire spinal section. D Representative western blots for GFAP, Iba1, vimentin, and CD68 in the lumbar spinal cord of untreated subjects and EAE mice treated with vehicle or nimodipine during the acute and peak phase of the disease. α-Tubulin and β-actin were used as internal standards. One-way ANOVA followed by the Bonferroni’s test was used for comparisons between experimental groups. Analysis consisted of at least four spinal cords per condition and each dot denotes the mean of one subject. Values are presented as mean ± SEM ^p < 0.05, ^^p < 0.01, ^^^p < 0.001 versus untreated; *p < 0.05, **p < 0.01, ***p < 0.001 versus vehicle