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. 2019 Aug 8;9:11519. doi: 10.1038/s41598-019-47993-w

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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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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KUS121 prevents ATP depletion and endoplasmic reticulum (ER) stress. (a) Measurement of ATP concentration. Primary cortical neurons were exposed to vehicle (dimethyl sulfoxide, DMSO) or 100 μM KUS121 under control conditions or under OGD for 1.5 h. Then, ATP was measured (n = 6; *p < 0.05). (b) Left: Western blot analyses on CCAAT/enhancer-binding protein homologous protein (CHOP) and valosin-containing protein (VCP). Primary cortical neurons were treated with 0.25 μg/mL tunicamycin for 6 h with vehicle (DMSO) or 100 μM KUS121 and then subjected to western blot analyses. Right: Graph showing the ratio of CHOP to β-actin expression levels (n = 4; *p < 0.05).