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. 2021 Nov 12;38(6):927–943. doi: 10.1007/s10565-021-09677-y

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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/.

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Fig. 2 — Sevoflurane exposure in the developing brain could induce neuroapoptosis via the JNK/c-JUN/AP-1 axis, ERK1/2 MAPK axis, ERK1/2-NRF2/BACH1axis, PI3K/AKT axis, and CREB inactivation, which may downregulate the transcription of anti-apoptotic genes (BCL-2, BCL-XL, MCL1) and increase the levels of pro-apoptotic factors (BAX/BAK). This induces mitochondrial outer membrane permeabilization, promoting release of cytochrome C from the mitochondria, activating caspase-9 cleavage and informed apoptosome, resulting in caspase 3 activation and neuroapoptosis