RETRACTED: Inhibition of miR-495-3p ameliorated sevoflurane induced damage through BDNF/ERK/CREB signaling pathways in HT22 cells

Abstract

ObjectiveSevoflurane is used in anesthesia for surgery including in organ transplantation. We investigated the role of a non-coding single-stranded microRNA, miR-495-3p, in the sevoflurane-induced neurotoxicity using a mouse hippocampal neuronal cell line (HT22). MethodsThe levels of miR-495-3p in sevoflurane-exposed mice and HT22 cells were determined via RT-qPCR. The role of miR-495-3p on cell viability and apoptosis were determined by CCK-8 and flow cytometric assay, respectively. Western blotting was explored to measure levels of Bax, Bcl-2, active caspase 3, BDNF, p-ERK/ERK and p-CREB/CREB in HT22 cells. ELISA assay was used to examine the levels of reactive oxygen species (ROS), superoxide dismutase (SOD) and glutathione peroxidase (GPX) in cells. Dual luciferase reporter assay was used to explore the interaction of miR-495-3p and BDNF. ResultsThe level of miR-495-3p was increased sevoflurane-exposed mice and in sevoflurane-treated HT22 cells. Downregulation of miR-495-3p inhibited sevoflurane-induced apoptosis and promoted cell proliferation by upregulating the proteins of Bcl-2 and downregulating the expressions of Bax and active caspase-3 in HT22 cells. In addition, inhibition of miR-495-3p alleviated sevoflurane-induced oxidative injuries in HT22 cells via decline of ROS and upregulation of SOD and GPX. MiR-495-3p can inhibit the ERK/CREB pathway by targeting BDNF. ConclusionDownregulation of miR-495-3p can decrease oxidative status in HT22 cells and alleviate sevoflurane-induced cytotoxicity through stimulating the BDNF/ERK/CREB pathway.