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. 2021 Oct 13;18:226. doi: 10.1186/s12974-021-02289-7

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© The Author(s) 2021

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. 3 — Representative immunofluorescence staining of GPR39 and the microglia marker Iba-1 in the brain at 48-h post-HIE. GPR39 was co-localized with Iba-1 in the sham (A), vehicle (B), and TC-G 1008 treatment (15 mg/kg) group (C), respectively. Compared with the sham group, GPR39 (green) expression was increased on microglia (red) in vehicle group and further increased post-TC-G 1008 treatment. Blue was for nucleus (DAPI). D Quantitative analysis of GPR39-positive Iba-1 cells in the ipsilateral cortex at 48-h post-HIE. E The schematic diagram shows the location of immunofluorescence staining (small white box). (Data are represented as mean ± SD; *p < 0.05 vs. sham; ^#p < 0.05 vs. HIE + vehicle; n = 4/group; scale bar = 50 μm)