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. 2020 Jun 12;17:184. doi: 10.1186/s12974-020-01861-x

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© The Author(s) 2020

Open AccessThis 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/. 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 in a credit line to the data.

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Fig. 3 — The effect of iP inhibition on regional astrocyte death, ROS production, oxidatively damaged and poly-ubiquitinated protein load. a–e Human brainstem and spinal cord astrocytes were stimulated with or without 10 ng/ml IFNγ and/or ONX 0914 for 48 h. a Caspase activity and b ROS were measured and normalized to live cells. c Protein lysate was collected and derivatized, and (d) oxidatively damaged protein accumulation was quantified and normalized to β-actin levels. e Protein lysate was probed for Lys48-labeled poly-ubiquitinated proteins, normalized to β-actin expression, and (f) quantified. Data represent the mean ± SEM from 3 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 by 2-way ANOVA. ROS reactive oxygen species, Ox-damaged oxidatively damaged