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. 2020 Jan 29;17:40. doi: 10.1186/s12974-020-1709-8

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© The Author(s). 2020

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. 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.

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Fig. 5 — Effect of MK-deficiency on neuronal apoptosis activity after TBI. Caspase-3-positive cells were detected in the lesion and perilesional areas (a). A higher expression of the caspase-3-positive area was seen in Mdk^−/− than in the Mdk^+/+ mice at 7 days after TBI (b). Moreover, caspase-3-immuno-positive cells co-localized with a neuronal marker (NeuN), indicating neuronal apoptosis surrounding the lesion at 7 days after TBI (c). The populations of apoptotic neurons (arrow) were significantly lower in Mdk^−/− than in Mdk^+/+ mice (d). Data are presented as mean ± SE (n = 5 mice/group). *p < 0.05 (comparison with MK^+/+ and Mdk^−/−). ##p < 0.01 (comparison with 3 days and 14 days). Scale bar = 50 μm (all panels of a) and 25 μm (all panels of c)