沉默CircHIPK3可通过增强miR-338-3p改善七氟醚探索中的学习和记忆功能障碍以及神经损伤。

IF 2.2 4区 医学 Q3 TOXICOLOGY Toxicology Research Pub Date : 2024-08-19 eCollection Date: 2024-08-01 DOI:10.1093/toxres/tfae132
Xiuli Li, Xuefei Li, Yinan Liang
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引用次数: 0

摘要

背景:七氟烷(Sev七氟醚(Sev)是一种广泛使用的挥发性麻醉剂,可引起神经毒性,并损害学习和记忆:本研究探讨circHIPK3在Sev暴露的神经毒性和学习记忆损伤中的作用和机制:方法:将 SD 大鼠和海马神经元细胞暴露于 Sev。RT-qPCR分析circHIPK3和miR-338-3p的水平。进行MWM测试以检测大鼠的行为变化。使用 RT-qPCR 分析 circHIPK3 和 miR-338-3p 的水平。通过 ELISA 检测分析促炎因子的表达。CCK-8、流式细胞术和商用 ROS 检测试剂盒用于检测细胞活力、凋亡和 ROS 生成。DLR和RIP检测验证了circHIPK3与miR-338-3p的结合:与对照组相比,Sev 增加了大鼠海马组织和神经细胞中 circHIPK3 的表达,但降低了 miR-338-3p 的水平。此外,沉默大鼠的 circHIPK3 可减轻 Sev 诱导的学习和记忆功能下降。减少 circHIPK3 可部分逆转 Sev 诱导的细胞活力下降、细胞凋亡增加和 ROS 过度产生。然而,下调 miR-338-3p 后,circHIPK3 对 Sev 神经毒性的抑制作用得以恢复:总之,沉默circHIPK3可通过增强miR-338-3p的表达缓解Sev暴露诱导的学习和记忆缺陷以及神经毒性。
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Silencing CircHIPK3 improves sevoflurane-explore learning and memory dysfunction and nerve damage via enhancing miR-338-3p.

Background: Sevoflurane (Sev), a widely used volatile anesthetic, can cause neurotoxicity, and impair learning and memory.

Objective: This study investigates the role and mechanisms of circHIPK3 in Sev-exposed neurotoxicity and learning and memory impairment.

Methods: SD rats and hippocampal neuronal cells were exposed to Sev. RT-qPCR analysis of circHIPK3 and miR-338-3p levels. MWM test was performed to examine the behavioral changes in rats. The levels of circHIPK3 and miR-338-3p levels were investigated using RT-qPCR. ELISA assay to analyze the expression of pro-inflammatory factors. CCK-8, flow cytometry, and commercial ROS assay kits were analyzed to detect cell viability, apoptosis, and ROS production. DLR and RIP assays validate circHIPK3 binding to miR-338-3p.

Results: Sev increased circHIPK3 expression in rat hippocampal tissue as well as in neuronal cells but decreased miR-338-3p levels compared to controls. circHIPK3 binding to miR-338-3p. Furthermore, silencing of circHIPK3 rats attenuated Sev-induced decline in learning and memory functions . silencing circHIPK3 also reduced Sev-induced secretion of inflammatory factors in rat and neuronal cells. Reducing circHIPK3 partially reversed the Sev-induced decrease in cell viability, increased apoptosis, and overproduction of ROS. However, the inhibitory effect of circHIPK3 on Sev neurotoxicity was restored upon downregulation of miR-338-3p.

Conclusion: Collectively, silencing circHIPK3 alleviates Sev exposure-induced learning and memory deficits and neurotoxicity by enhancing miR-338-3p expression.

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Toxicology Research
Toxicology Research TOXICOLOGY-
CiteScore
3.60
自引率
0.00%
发文量
82
期刊介绍: A multi-disciplinary journal covering the best research in both fundamental and applied aspects of toxicology
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