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. 2018 Oct 8;9:4126. doi: 10.1038/s41467-018-06505-6

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — ISP promotes functional and histological recovery in EAE mouse model. a Diagram of ISP administration to EAE mice at the beginning or the peak of sickness determined by clinical score (Created by F.L. and A.P.T.). b Clinical score of disease severity in MOG_35-55-induced EAE mice treated with ISP or vehicle daily beginning at the onset or the peak of disease. c Mean improvement in disease score per animal of EAE cohort in B (n = 9 (EAE vehicle group), 15 (EAE ISP onset group) and 12 (EAE ISP peak group), ANOVA F(2,33) = 20.96; Tukey’s multiple comparison test, P_{EAE+Veh versus EAE ISP onset} < 0.0001, P_{EAE+Veh versus EAE ISP peak} = 0.0004). d, e Luxol fast blue (LFB) staining of myelin, demonstrating normal myelin integrity in ISP-treated EAE mice at 48 days post induction, in contrast to the marked loss of myelin present in the spinal cord of vehicle-treated control (n = 5 mice/group, P = 0.0002, t = 6.647, df = 8; Two-tailed unpaired Student’s t test). Dashed lines demarcate lesion areas. Scale bar = 100 μm. f Double immunostaining for MBP and neurofilament-200 (NF200) in the thoracic spinal cord of vehicle- and ISP-treated EAE mice at 48 days post induction. Dashed lines demarcate lesion areas. Scale bar = 100 μm. g Western blot analysis of MBP expression in spinal cord tissue of vehicle or ISP-treated control mice and EAE mice at 48 days post induction. Data are normalized to β-actin protein expression (n = 4 mice/group, ANOVA F(3,12) = 26.68; Tukey’s multiple comparison test, P_{con versus EAE+Veh} = 0.0001, P_{EAE+Veh versus EAE+ISP} = 0.0037). h Electron micrographs from ventral lumbar spinal cords of vehicle and ISP-treated EAE mice 48 days following induction. Scale bar = 2 μm. i Number of myelinated axons in the spinal cord lesions of vehicle and ISP-treated EAE mice (n = 3 mice/group, P = 0.0014, t = 7.815, df = 4; two-tailed unpaired Student’s t test). j Quantification of the g-ratios (axon diameter/fiber diameter) of myelinated fibers in the ventral lumbar spinal cords of vehicle and ISP-treated EAE mice (EAE + Veh group, g-ratio = 0.8874 ± 0.001901; EAE + ISP group, g-ratio = 0.8423ISP group; n = 134 remyelinated axons from three mice/group; P < 0.0001, t = 14.31, df = 266; two-tailed unpaired Student’s t test). The data are presented as mean ± s.e.m. *P < 0.05, **P < 0.01, ***p < 0.001