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. 2020 May 30;17:171. doi: 10.1186/s12974-020-01845-x

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 8 — JNK and P38 phosphorylation were restrained by CD200Fc after OGD in BV2 cells. CD200Fc inhibited phosphorylation of JNK (a, b) and P38 (a, c). Results are expressed as means ± SEM. ^#P < 0.05, ^##P < 0.01, ^###P < 0.001 versus the control group. ^**P < 0.05, ^**P < 0.01, ^***P < 0.001 versus the OGD+IgG group. CD200Fc reversed the phosphorylation of JNK (d, e) and P38 which induced by anisomycin (an agonist of JNK and P38) (d, f), n = 3. Results are expressed as means ± SEM. ^#P < 0.05, ^##P < 0.01, ^###P < 0.001 versus the control group. ^**P < 0.05, ^**P < 0.01, ^***P < 0.001 versus the anisomycin+IgG group.