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. 2021 Jun 14;11:12497. doi: 10.1038/s41598-021-91507-6

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© The Author(s) 2021

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 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/.

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Effect of selumetinib on acrolein-induced oxidative stress. (A) Primary cultured cortical neurons were treated with acrolein (0–30 μM). (B,C) Primary cultured cortical neurons were treated with acrolein (30 μM) with/without selumetinib (SEL, 10 μM) for 24 h. Western blot assay was employed to measure HO-1 (A), Nrf-2 (B) and HO-1 (C). Each lane contained 30 μg protein for all experiments. Graphs show statistical results from relative optical density of bands on the blots. Values are the mean ± SEM (n = 3/treatment). *p < 0.05 statistically significant in the acrolein groups compared with the control groups; ^#p < 0.05 statistically significant in acrolein plus SEL group compared with acrolein group by one-way analysis of variance (one-way ANOVA) and followed by the LSD test as post-hoc method.