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. 2020 Feb 15;17:57. doi: 10.1186/s12974-019-1662-6

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© The Author(s). 2020

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 9 — Clemastine improves axonal hypomyelination via inhibition of p38 phosphorylation in microglial cells. Panel a showing phosphorylation-p38 (38 kDa) and total-p38 (38 kDa) immunoreactive bands. Panel b is bar graph which indicates that expression of p-p38 were improved in the AMCs after OGD administration for 1 h. The clemastine and MCC950 may attenuate the increment. Panel c showing IL-1β (17 kDa), NLRP3 (62 kDa), and β-actin (42 kDa) immunoreactive bands. Panels d and e are bar graphs showing the expression of IL-1β and NLRP3 were significantly up-regulated at 1 h after treatment with OGD compared with the controls. Clemastine could reduce the high expressions of NLRP3 and IL-1β proteins by inhibiting the p-p38. The inhibition was strengthened after adding additional MCC950 or SB203580 (a specific p38 pathway inhibitor). Panel f showing MBP (32 kDa), CNPase (48 kDa), and β-actin (42 kDa) immunoreactive bands. Panels h and g are bar graphs showing the protein expressions of MBP and CNPase were significantly downregulated at 7 days after OGD compared with the controls. Clemastine and SB203580 could upregulate the expressions of MBP and CNPase proteins induced by OGD by inhibiting the p-p38. When additional MCC950 or SB203580 was added, the expression of MBP was upregulated compared with the OGD + clemastine group. N=3. *P < 0.05