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.

中文翻译：

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LncRNA牛磺酸上调基因1参与异氟醚诱导的神经毒性

背景

异氟醚（ISO）具有诱导和恢复快的特点，已成为世界上最常用的吸入麻醉药之一。

客观的

本研究的目的是通过体外细胞实验探索异氟醚（ISO）中长链非编码RNA牛磺酸上调基因1（TUG1）诱导神经毒性的生物学机制。

结果

ISO 暴露抑制细胞活力，同时通过上调长链非编码 RNA (lncRNA) TUG1 促进 HT22 细胞中 ROS 的产生、细胞凋亡和炎性细胞因子的释放。MiR-15a-5p 是 TUG1 的直接靶点，并被 TUG1 反向调控。miR-15a-5p 的过表达减轻了 ISO 暴露诱导的神经毒性，而 TUG1 的下调通过 miR-15a-5p 的上调减轻了 ISO 暴露诱导的神经毒性。

结论

TUG1 的下调减少了 ISO 诱导的 ROS 生成、神经元细胞凋亡和炎症反应。HT22 细胞中 ISO 诱导的神经毒性受 TUG1/miR-15a-5p 轴调节。