GRIA1 Alleviates Sevoflurane-Induced Neurotoxicity by Suppressing Autophagy

The neurotoxicity caused by inhaled anesthetics has attracted more attention. Sevoflurane (SEV), a common general anesthetic, has a wide range of clinical applications. However, the underlying molecular mechanism of SEV-induced neurotoxicity is blurry.Cell viability and apoptosis were evaluated using CCK-8 and flow cytometry. The abundances of targeted molecules were measured using RT-qPCR, western blot and IF assay. SEV induction reduced cell viability, promoted cell apoptosis and autophagy of HT22 cells, which was positively related with gradually increasing concentrations of SEV. In addition, Glutamate ionotropic receptor AMPA type subunit 1 (GRIA1) expression was evidently decreased by SEV induction and its overexpression abolished SEV-mediated influences on cell viability, apoptosis and autophagy of HT22 cells. Furthermore, the autophagy inducer rapamycin reversed GRIA1 overexpression-mediated promotion of cell viability and suppression of cell apoptosis and autophagy of HT22 cells upon SEV induction. GRIA1 improved SEV-induced neurotoxicity by suppressing autophagy.