七氟醚诱导发育神经毒性机制的新见解

IF 3 4区医学 Q2 GENETICS & HEREDITY

Epigenomics Pub Date : 2024-01-01 Epub Date: 2024-09-24 DOI:10.1080/17501911.2024.2395250

Tingting Gao, Zeqing Huang

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引用次数: 0

摘要

目的：本研究通过转录组测序和模型探讨七氟醚（Sevo）诱导的新生儿神经毒性机制：方法：将 7 天大的小鼠暴露于 3% 的 Sevo，收集海马组织，分析与正常小鼠相比有差异表达的 lncRNA 和 mRNA。选择了 MiR-152-3p，并在 BV2 小胶质细胞和小鼠海马神经元中探讨了 H19、USP30 和 miR-152-3p 之间的相互作用：结果：Sevo 通过 USP30 上调破坏线粒体自噬，加剧神经毒性并激活 NLRP1 炎症体介导的炎症：Sevo的神经毒性是通过H19/miR-152-3p/USP30轴介导的，这与小胶质细胞对神经元自噬的调控有关。

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Novel insights into sevoflurane-induced developmental neurotoxicity mechanisms.

Aim: This study explores Sevoflurane (Sevo)-induced neurotoxicity mechanisms in neonates through transcriptome sequencing and models.Methods: Seven-day-old mice were exposed to 3% Sevo, and hippocampal tissue was collected for analysis of differentially expressed lncRNAs and mRNAs compared with normal mice. MiR-152-3p was selected, and the interaction between H19, USP30, and miR-152-3p was explored in BV2 microglial cells and mouse hippocampal neurons.Results: Sevo disrupts mitochondrial autophagy via USP30 upregulation, exacerbating neurotoxicity and activating NLRP1 inflammasome-mediated inflammation.Conclusion: Sevo neurotoxicity is mediated through the H19/miR-152-3p/USP30 axis, implicating microglial regulation of neuronal pyroptosis.

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来源期刊

Epigenomics GENETICS & HEREDITY-

CiteScore

5.80

自引率

2.60%

发文量

审稿时长

>12 weeks

期刊介绍： Epigenomics provides the forum to address the rapidly progressing research developments in this ever-expanding field; to report on the major challenges ahead and critical advances that are propelling the science forward. The journal delivers this information in concise, at-a-glance article formats – invaluable to a time constrained community. Substantial developments in our current knowledge and understanding of genomics and epigenetics are constantly being made, yet this field is still in its infancy. Epigenomics provides a critical overview of the latest and most significant advances as they unfold and explores their potential application in the clinical setting.