Long noncoding RNA small nucleolar RNA host gene 1 contributes to sevoflurane-induced neurotoxicity through negatively modulating microRNA-181b.

Sevoflurane has been reported to promote learning and memory disabilities by promoting neuroinflammation and neuroapoptosis. However, the precise mechanism by which sevoflurane mediating neurotoxicity remains to be determined. Cell viability, reactive oxygen species (ROS) generation, inflammation and apoptosis were measured by cell counting kit-8 assay, ROS kit, ELISA, flow cytometry and western blot assay. The abundance of small nucleolar RNA host gene 1 (SNHG1) and microRNA-181b (miR-181b) was measured by quantitative real-time PCR in HT22 cells. The binding sites between miR-181b and SNHG1 were predicted by Starbase, and this combination was verified by dual-luciferase reporter assay, RNA immunoprecipitation and RNA-pull down assays. Sevoflurane treatment promoted ROS generation, inflammation and apoptosis while impeded the viability of HT22 cells via upregulating long noncoding RNA (lncRNA) SNHG1. MiR-181b was a direct target of SNHG1, and it was inversely regulated by SNHG1 in HT22 cells. The overexpression of miR-181b counteracted the neurotoxicity of sevoflurane treatment in HT22 cells. MiR-181b depletion abolished the inhibitory effects of SNHG1 intervention on the ROS generation, inflammation and apoptosis and the promoting impact on the viability of HT22 cells. LncRNA SNHG1 contributed neurotoxicity in sevoflurane-stimulated HT22 cells via downregulating miR-181b. The SNHG1/miR-181b axis was a target for the prevention of sevoflurane-induced neurotoxicity.