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. 2020 Aug 31;17:257. doi: 10.1186/s12974-020-01921-2

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© The Author(s) 2020

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. 1 — Effects of rhFGF21 on infarct volumes and neurodeficits in the MCAO model. a Representative sample of brain slices with 2% TTC staining at 3 and 14 days after MCAO, and b quantification of the significant difference in the figure. n = 8. Values are mean ± SEM by unpaired t tests. c mNSS assessed at 1, 3, 7, and 14 days after MCAO. d–g Cumulative data illustrate the indicated neurobehavioral tests, including the time to contact (d) and the time to removal in the adhesive test (e) and results from the corner-turning test (f) and rotarod test (g) from day 1 to 14 after MCAO. n = 4 in the sham group, n = 10 in the MCAO and rhFGF21-treated group. Values are mean ± SEM by two-way ANOVA