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. 2023 Feb 16;20:6. doi: 10.1186/s12989-023-00517-x

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© The Author(s) 2023

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. 4 — Enhancement of brain edema after ischemic stroke by CRM28 exposure. CRM28 was suspended in water and intranasally (i.n.) administered at doses of 0, 10 or 100 µg/mouse once a day for 7 days. One day after induction of photothrombosis, T1WI and T2WI were obtained for each mouse by MRI, and then the infarct area was determined by TTC staining. A Representative images of T1WI, T2WI and TTC staining. B T2 hyperintense lesion (T2WI), TTC-unstained area (Infarct) and edema region (T2 hyperintense lesion except infarct) were quantified by ImageJ software. The values are presented as the mean ± S.D. (n = 5 animals in each group). The data were analyzed using one-way ANOVA [T2WI F(2, 12) = 9.124, p = 0.0039, Infarct F(2, 12) = 1.708, p = 0.2225, Edema F(2, 12) = 4.893, p = 0.0279] followed by Dunnett’s multiple comparisons test