HDAC3 deacetylates H3K27ac and H3K9ac on the TrkC promoter to exacerbate sevoflurane-induced neurotoxicity

Background Sevoflurane (Sev) is a widely used general anesthetic that can cause neurotoxicity. Histone acetylation is a vital epigenetic mechanism responding to environmental stresses. Objective This study was conducted to analyze the role of histone deacetylase 3 (HDAC3) in Sev-induced neurotoxicity and provide a theoretical reference for the treatment of anesthetic neurotoxicity. Results HDAC3 was upregulated in Sev-treated HT-22 cells. Inhibition of HDAC3 upregulated cell viability and downregulated apoptosis, oxidative stress and secretion of inflammatory cytokines. HDAC3 reduced H3K27ac and H3K9ac levels on the TrkC promoter to inhibit TrkC expression. TrkC downregulation reversed the alleviative role of si-HDAC3 in Sev-induced neurotoxicity. Conclusion HDAC3 enhanced Sev-induced neurotoxicity by reducing H3K27ac and H3K9ac to repress TrkC.