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. 2022 Jan 30;59(4):2580–2592. doi: 10.1007/s12035-021-02642-0

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© The Author(s) 2022

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/.

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Fig. 4 — Anti-inflammatory mechanisms of purpurin against ischemic damage in gerbils. A Levels of pro-inflammatory cytokines were measured 6 h and 4 days after ischemia in the gerbil hippocampus of control, vehicle, and 6 mg/kg purpurin groups (n = 5 per group). B Microglia and astrocytes were visualized to show the morphological changes after ischemia in the CA1 region of the control, vehicle, and purpurin groups with Iba-1 and GFAP immunohistochemical staining, respectively. In addition, NF-κB immunohistochemical staining was conducted in the hippocampal CA1 region. SO, stratum oriens; SP, stratum pyramidale; SR, stratum radiatum. Scale bar = 50 μm. Optical density was measured and expressed as a percentage of the value vs. control group (n = 5 per group). Data are expressed as mean value ± standard deviation and were analyzed using one-way ANOVA followed by Bonferroni’s post hoc test (^ap < 0.05, significantly different from the control group; ^bp < 0.05, significantly different from the vehicle group; ^cp < 0.05, significantly different from the group 6 h after ischemia)