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. 2021 Nov 10;8:58. doi: 10.1186/s40779-021-00353-0

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© The Author(s) 2021

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. 7 — Knockout of propofol FoxO1 or FoxO3a canceled the protective effects of propofol in attenuating the augmentation of ROS Levels caused by H/R injury under hyperglycemia (35 mmol/L). a ROS (reactive oxygen species) degrees measured by DHE (dihydroethidium) fluorescence staining (100 ×). b ROS levels detected by DCFH-DA (2, 7-dichlorodihydrofluorescein diacetate) fluorescence flow cytometry. c Statistical graph of DHE. d Statistical image of mean DCFH-DA fluorescence intensity. Data are mean ± SEM from three independent experiments each performed in triplicate. ^*P < 0.05, ^**P < 0.01