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. 2018 Jun 9;15:178. doi: 10.1186/s12974-018-1211-8

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© The Author(s). 2018

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 — LY294002 reversed the neuroprotection of exogenous Aggf1 after subarachnoid hemorrhage (SAH). a Pretreatment of LY294002 abolished the protective effects of rh-Aggf1 on neurological functions. b–e LY294002 reversed the effects of rh-Aggf1 against brain edema and BBB permeability and inflammatory response (albumin extravasation and MPO expression). c, f–l LY294002 reserved rh-Aggf1 induced changes in protein levels of PI3K, p-Akt, p-NF-κB p65, VE-cadherin, Occludin, claudin-5, TNF-α, and IL-1β in rh-Aggf1-treated rats after SAH. ^#P < 0.05 vs sham; *P < 0.05 vs vehicle; ^&P < 0.05 vs rh-Aggf1 and rh-Aggf1+DMSO. DMSO, dimethyl sulfoxide; LY294002, PI3K-specific inhibitor; MPO, myeloperoxidase