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. 2017 Sep 2;14:177. doi: 10.1186/s12974-017-0953-z

Fig. 2.

Fig. 2

Chronic phase glibenclamide reduces demyelination in EAE. White matter of lumbar spinal cord sections from non-EAE control (CTR), untreated EAE mouse (EAE), and EAE mouse treated with glibenclamide starting on pid-24 (EAE + G), stained with Luxol fast blue (LFB) (myelin) or immunolabeled for myelin basic protein (MBP) (myelin), CNPase (mature oligodendrocytes), PDGFR-α (oligodendrocyte progenitor cells; OPC) or SMI-312 (neurofilament marker), as indicated; nuclei stained with DAPI in the MBP sections; original magnification, × 200 (LFB) or × 400 (all immunolabelings); bar graphs: percent of quadrants with myelin loss by LFB staining, MBP immunolabeling, or CNPase immunolabeling; quantification of PDGFR-α-expressing OPC near the central canal; percent of quadrants with axonal loss by SMI-132 labeling; 5 mice/group; ## P < 0.01 with respect to non-EAE control (CTR); *P < 0.05 and **P < 0.01 with respect to untreated EAE; scale bars, 100 μm