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. 2019 Nov 28;16:243. doi: 10.1186/s12974-019-1641-y

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© The Author(s). 2019

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. 9 — As innate immune cells in the CNS, microglia are activated after SAH in vivo and in vitro. Microglia then initiate an inflammatory cascade to aggravate neuronal damage, which is an important cause of EBI. A neurosteroid, DHEA, exerts an anti-inflammatory effect after Hb exposure by initiating the TrkA/Akt signalling pathway and inducing the expression of the H3K27me3 demethylase, Jmjd3. Jmjd3 then negatively regulates proinflammatory genes and modulates the proinflammatory/anti-inflammatory switch, possibly through its downstream transcription factors