USP18 alleviates neurotoxicity induced by sevoflurane via AKT and NF-κB pathways

BackgroundSevoflurane 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.ObjectiveTo 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.ResultsUSP18 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.ConclusionUSP18 was involved in the pathology of sevoflurane-induced neurotoxicity.