The protective effects of miR-128-3p on sevoflurane-induced progressive neurotoxicity in rats by targeting NOVA1

MiR-128 is highly expressed in the central nervous system and may regulate the directional differentiation of bone marrow stromal stem cells into nerve cells. However, its role and mechanism in sevoflurane-induced progressive neurotoxicity in rats are rarely reported. Therefore, this study aims to explore the protection of miR-128-3p on sevoflurane-induced neurotoxicity. Hippocampal neurons were isolated and sevoflurane was used to treat the cells. Cell counting kit-8 (CCK-8) was used to detect cell viability. Immunofluorescence was used to detect enrichment of GFAP or beta III tubulin to identify nerve cells. Dual luciferase assay was used to identify the targeted binding relationship between miR-128-3p and NOVA1. The effect of miR-128-3p and sevoflurane on cells regarding apoptosis was detected by flow cytometry. The expression of apoptosis-related protein and oxidative stress-related proteins were detected by western blot. Enzyme-linked immuno-sorbent assay (ELISA) was used to measure inflammatory cytokine levels. Hippocampal neurons' cell viability was significantly decreased by treatment with sevoflurane. MiR-128-3p was down-regulated after sevoflurane treatment in cells. Overexpressed miR-1283p partially reversed the role of sevoflurane treatment in triggering cell apoptosis, enhancing the expression of Bax and cleaved caspase-3 and inhibiting Bcl-2 expression obviously. Overexpressed miR-128-3p partially reversed the role of sevoflurane treatment in promoting the expression of NOXland NOX4, and inflammatory cytokine levels by targeting with NOVA1. MiR-128-3p might be a potential therapeutic target for the prevention or treatment of sevoflurane-induced neurotoxicity by targeting with NOVA1.