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LncRNA taurine up-regulated gene 1 participates in isoflurane induced neurotoxicity
Zhang Faqiang,Chen Guoqing,Wang Long,Feng Zeguo,Mi Weidong 대한독성 유전단백체 학회 2021 Molecular & cellular toxicology Vol.17 No.3
Background Isoflurane (ISO), with the characteristics of rapid induction and recovery, has become one of the most commonly used inhalation anesthetics in the world. Objective 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. Result 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. Conclusion 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. Background Isoflurane (ISO), with the characteristics of rapid induction and recovery, has become one of the most commonly used inhalation anesthetics in the world. Objective 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. Result 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. Conclusion 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.