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. 2020 Sep 10;10:14906. doi: 10.1038/s41598-020-72023-5

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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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Inhibition of AhR activation by TMF treatment (A) Representative merged images of AhR, NeuN, and 4′,6-diamidino-2-phenylindole (DAPI) staining of the PIR 24 h after ischaemia (upper row, magnification × 630). Yellow boxes indicate the regions displayed at higher magnification from the middle row (scale bar = 20 μm). The bottom row shows photomicrographs of AhR signal intensity, which are enlarged versions of the white boxes in the middle row. The red dotted lines outline the nucleus. (B) The signal intensity of nuclear AhR in the control group was significantly higher than that in the sham and TMF treatment groups. **P < 0.01 vs. sham group; ^#P < 0.05 vs. control group.