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. 2019 Dec 6;11(4):678–688. doi: 10.1007/s12975-019-00757-0

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© The Author(s) 2019

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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Fig. 3 — C5 antibody treatment reduces brain injury in experimental subarachnoid hemorrhage. a Representative images of mouse cortex stained with antibody against Iba-1 (orange); cell nuclei in blue (Hoechst). b Representative images of mouse cortex stained with antibody against cleaved caspase 3 (CC3; green); NeuN (red) and cell nuclei in blue (Hoechst). c C5a receptor deficient (C5aR^−/−) and wild-type mice treated with C5-specific antibodies had a > 38% reduction in microglia/macrophage activation compared to untreated wild-type mice. Kruskal-Wallis, Dunn’s post hoc. d C5aR^−/− mice and control BALB/c mice treated with C5-specific monoclonal antibodies had > 39% reduction in cells undergoing apoptosis, compared to untreated wild-type mice 48 h after subarachnoid hemorrhage. Kruskal-Wallis, Dunn’s post hoc; n = 15 mice per group; ****p ≤ 0.0001, ***p ≤ 0.001, *p ≤ 0.05; mean ± SD; scale bars 30 μm.