Isoflurane (ISO), with the characteristics of rapid induction and recovery, has become one of the most commonly used inhalation anesthetics in the world.
The purpose of this study was to explore the biological mechanism of long non-coding RNA taurine up-regulated gene 1 (TUG1) in isoflurane (ISO) induced neurotoxicity through in vitro cell experiments.
ISO exposure inhibited cell viability while promoted ROS generation, cell apoptosis and inflammatory cytokines release in HT22 cells via upregulating long noncoding RNA (lncRNA) TUG1. MiR-15a-5p was a direct target of TUG1 and was reversed regulated by TUG1. Overexpression of miR-15a-5p alleviated neurotoxicity induced by ISO exposure, while downregulation of TUG1 alleviated the neurotoxicity induced by ISO exposure via upregulation of miR-15a-5p.
Downregulation of TUG1 reduced ISO-induced ROS generation, neuron cell apoptosis and inflammatory response. ISO-induced neurotoxicity in HT22 cells was regulated by TUG1/miR-15a-5p axis.