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. 2020 May 4;38(4):979–991. doi: 10.1007/s12640-020-00203-2

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© The Author(s) 2020

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 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/.

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Fig. 4 — The effects of 8-OaS on inflammation in the mouse BLA during CFA-induced chronic inflammatory pain. a After 14 days, the brain slices containing BLA were immunostained with microglial marker Iba-1 antibody (red), and nuclei were stained with Hoechst33258 (blue). Scale bar = 20 μm. b 8-OaS inhibited the activation of microglia in the BLA of CFA-injected mice and had a dose-dependent effect. 8-OaS decreased the elevated levels of c IL-1β, d IL-6, and e TNF-a in the BLA on day 14 after CFA injection. Each value represents the mean ± SEM of three independent experiments (n = 6, *p < 0.05, **p < 0.01 versus the control group; ^#p < 0.05, ^##p < 0.01 versus the CFA-injected group)