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. 2020 Jun 15;17:187. doi: 10.1186/s12974-020-01841-1

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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. 9 — ELISA tests to evaluate inflammation-related cytokines with OXA treatment. The levels of pro-inflammatory cytokines including a IL-1β, b TNFα, c IL-6, and d IL-12 were significantly downregulated with OXA treatment, and the levels of anti-inflammatory cytokines including e IL-4 and f IL-10 were significantly upregulated with OXA treatment evaluated at 24 h after ICH. The effects of OXA were reversed by CaMKKβ inhibitor (STO-609) and OXR2 inhibitor (JNJ-10397049) but not OXR1 inhibitor (SB-334867). One-way ANOVA, *p < 0.05 vs. sham group, #p < 0.05 vs. vehicle group, @p < 0.05 vs. OXA group. Error bars represent mean ± SD, n = 6 per group