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. 2020 Jun 10;17:182. doi: 10.1186/s12974-020-01862-w

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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 — CSF1R inhibitor BLZ945 abolished the anti-inflammatory effects of rh-CSF1 via CSF1R/PLCG2/PKCε/CREB signaling pathway at 48 h after HI. a Representative western blot bands. b–i Densitometric quantification of p-CSF1R, CSF1R, CSF1, p-PLCG2/PLCG2, p-PKCε/PKCε, p-CREB/CREB, IL-1β and TNF-α in the ipsilateral hemisphere showed that rh-CSF1 treatment upregulated the levels of p-CSF1R, p-PLCG2, p-PKCε, and p-CREB, leading to less pro-inflammatory cytokines of IL-1β and TNF-α. BLZ945 significantly abolished such effects when administered with rh-CSF1. *P < 0.05 vs. sham; ^#P < 0.05 vs. HI+ Vehicle; ^@P < 0.05 vs. HI+ rh-CSF1 + DMSO; Data are represented as mean ± SD, n = 6 in each group