Abstract
Background
Sevoflurane has obvious side effects during anesthesia, which caused neuronal apoptosis and neuroinflammation. How to reduce sevoflurane-induced neurotoxicity is an urgent problem to be solved.
Objective
To assess the role of USP18 in anesthetic sevoflurane-induced neurotoxicity, detect its effects on neuroinflammation, oxidative stress, and apoptosis, and explore the related potential signaling pathway.
Results
USP18 alleviated sevoflurane-induced learning and memory dysfunction and changed distribution of neurons. USP18 also reduced sevoflurane-induced neuroinflammation. We further found that USP18 reduced the sevoflurane-induced oxidative stress in the mice model. USP18 also attenuated sevoflurane-induced neuronal apoptosis. Mechanically, USP18 reduced sevoflurane-induced neurotoxicity via AKT and NF-κB pathway.
Conclusion
USP18 was involved in the pathology of sevoflurane-induced neurotoxicity.
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FW and YY designed the study and supervised the data collection; YW analyzed the data and interpreted the data; YL prepared the manuscript for publication and reviewed the draft of the manuscript. All the authors have read and approved the manuscript.
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The author Fengjuan Wang declares that he/she has no conflict of interest. The author Yu Yao declares that he/she has no conflict of interest. The author Yinghui Wu declares that he/she has no conflict of interest. The author Yan Lu declares that he/she has no conflict of interest.
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Wang, F., Yao, Y., Wu, Y. et al. USP18 alleviates neurotoxicity induced by sevoflurane via AKT and NF-κB pathways. Mol. Cell. Toxicol. 18, 431–438 (2022). https://doi.org/10.1007/s13273-021-00217-7
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DOI: https://doi.org/10.1007/s13273-021-00217-7