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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. 3 — Sevoflurane could induce neurodegenerative in the developing brain through multiple signaling pathways such as PTP-1B/ER axis, CREB/BDNF/SIRT1 axis, SIRT 2/microglia activation, and HDAC6 overexpression. Sevoflurane exposure suppressed p-AKT/AKT and mTOR, increasing the level of Beclin-1 and LC3-II/LC3-I and decreasing the levels of sequestosome 1 and p62, which induce activation of autophagy. Autophagy could induce neurodegenerative, which involved in sevoflurane-induced neurodegenerative