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. 2020 Nov 19;10:20233. doi: 10.1038/s41598-020-75450-6

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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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SHRs display increases in markers of neuronal damage following stroke that are not increased in normotensive animals. (A) Representative image for Western blot data. (B) Stroked SHR show increase in HMGB1 (p (interaction) < 0.05, 2-way ANOVA). (n = 4–8, per group). (C) and (D) Stroked SHRs show increase in activated MMP9 (p (interaction) < 0.01 for upper band and < 0.001 for lower band, 2-way ANOVA). Stroked SHRs show an increase of activated MMP9 (p < 0.05 for upper band and < 0.01 for lower band, Bonferroni post-hoc test) (n = 4–8, per group). (E) SHR show increase in full-length PARP1 after stroke (p (interaction) < 0.01, 2-way ANOVA). Stroked SHR show an increase of PARP1 compared to stroked Wistars (p < 0.05, Bonferroni post-hoc test) (n = 4–8, per group). (a,b: Tukey post-hoc multiple comparisons, pairs of means with different letters are significantly different).