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. 2022 May 31;10:82. doi: 10.1186/s40168-022-01271-6

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© The Author(s) 2022

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 — 3-HPA and 4-HBA mediate cardiac protection through activating NRF2. A, B 3-HPA (100 μM, 24 h) reduced the percentage of TUNEL staining positive cardiomyocytes (n = 6:6:6:6), Bax/Bcl₂, cleaved Caspase3/Caspase3, NRF2 (n = 3:3:3:3) in NRCMs under oxygen glucose deprivation/reperfusion (OGD/R). C, D 4-HBA (100 μM, 24 h) decreased the percentage of TUNEL staining positive cardiomyocytes (n = 6:6:6:6), Bax/Bcl₂, cleaved Caspase3/Caspase3, NRF2 (n = 3:3:3:3) in NRCMs under OGD/R. E, F Inhibition of NRF2 increased the percentage of TUNEL staining positive cardiomyocytes decreased by 3-HPA and 4-HBA in NRCMs under OGD/R (n = 6:6:6:6). Scale bar: 100 μm. Data were represented as mean ± SD. Significant differences were assessed by two-way ANOVA followed by Bonferroni's multiple comparisons test. *p < 0.05, **p < 0.01, ***p < 0.001 versus respective control