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Dexmedetomidine regulates sevoflurane-induced neurotoxicity through the miR-330-3p/ULK1 axis
Journal of Biochemical and Molecular Toxicology ( IF 3.6 ) Pub Date : 2021-09-30 , DOI: 10.1002/jbt.22919
Shan Xu 1 , Ruyue Gao 1 , Liang Chen 1
Affiliation  

Sevoflurane (Sev), a widely used volatile anesthetic, can cause long-term neurotoxicity and learning and memory impairment. Dexmedetomidine (Dex) has been reported to exhibit neuroprotective effects in numerous neurological disorders. Our work aimed to evaluate the molecular mechanisms of Dex in Sev-induced neurotoxicity. In this study, it was found that Dex mitigated Sev-induced neurotoxicity. Moreover, Sev treatment upregulated the miR-330-3p expression in hippocampus tissues, while this effect was reversed by the Dex treatment. Additionally, microRNA-330-3p (miR-330-3p) inhibition was verified to inhibit cell apoptosis and facilitate mitophagy. ULK1 was confirmed as a downstream target of miR-330-3p and miR-330-3p could negatively regulate ULK1 expression. Finally, the effects of miR-330-3p inhibition on Sev-induced neurotoxicity could be offset by ULK1 knockdown or further intensified by Dex treatment. In summary, our study demonstrated that Dex regulated cell apoptosis and mitophagy in Sev-induced neurotoxicity through the miR-330-3p/ULK1 axis. These findings might provide novel insights into the treatment of Sev-induced neurotoxicity.

中文翻译:

右美托咪定通过 miR-330-3p/ULK1 轴调节七氟醚诱导的神经毒性

七氟醚 (Sev) 是一种广泛使用的挥发性麻醉剂,可引起长期神经毒性和学习记忆障碍。据报道,右美托咪定 (Dex) 在许多神经系统疾病中表现出神经保护作用。我们的工作旨在评估 Dex 在 Sev 诱导的神经毒性中的分子机制。在这项研究中,发现 Dex 减轻了 Sev 诱导的神经毒性。此外,Sev 治疗上调了海马组织中 miR-330-3p 的表达,而 Dex 治疗逆转了这种作用。此外,证实抑制 microRNA-330-3p (miR-330-3p) 可抑制细胞凋亡并促进线粒体自噬。ULK1 被证实是 miR-330-3p 的下游靶标,并且 miR-330-3p 可以负调节 ULK1 的表达。最后,miR-330-3p 抑制对 Sev 诱导的神经毒性的影响可以被 ULK1 敲低抵消或通过 Dex 治疗进一步加强。总之,我们的研究表明,Dex 通过 miR-330-3p/ULK1 轴调节 Sev 诱导的神经毒性中的细胞凋亡和线粒体自噬。这些发现可能为 Sev 诱导的神经毒性的治疗提供新的见解。
更新日期:2021-09-30
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