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
{"title":"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。","authors":"Xiuli Li, Xuefei Li, Yinan Liang","doi":"10.1093/toxres/tfae132","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Sevoflurane (Sev), a widely used volatile anesthetic, can cause neurotoxicity, and impair learning and memory.</p><p><strong>Objective: </strong>This study investigates the role and mechanisms of circHIPK3 in Sev-exposed neurotoxicity and learning and memory impairment.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>Collectively, silencing circHIPK3 alleviates Sev exposure-induced learning and memory deficits and neurotoxicity by enhancing miR-338-3p expression.</p>","PeriodicalId":105,"journal":{"name":"Toxicology Research","volume":"13 4","pages":"tfae132"},"PeriodicalIF":2.2000,"publicationDate":"2024-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11331635/pdf/","citationCount":"0","resultStr":"{\"title\":\"Silencing CircHIPK3 improves sevoflurane-explore learning and memory dysfunction and nerve damage via enhancing miR-338-3p.\",\"authors\":\"Xiuli Li, Xuefei Li, Yinan Liang\",\"doi\":\"10.1093/toxres/tfae132\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Sevoflurane (Sev), a widely used volatile anesthetic, can cause neurotoxicity, and impair learning and memory.</p><p><strong>Objective: </strong>This study investigates the role and mechanisms of circHIPK3 in Sev-exposed neurotoxicity and learning and memory impairment.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>Collectively, silencing circHIPK3 alleviates Sev exposure-induced learning and memory deficits and neurotoxicity by enhancing miR-338-3p expression.</p>\",\"PeriodicalId\":105,\"journal\":{\"name\":\"Toxicology Research\",\"volume\":\"13 4\",\"pages\":\"tfae132\"},\"PeriodicalIF\":2.2000,\"publicationDate\":\"2024-08-19\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11331635/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Toxicology Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1093/toxres/tfae132\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/8/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"TOXICOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicology Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/toxres/tfae132","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/8/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"TOXICOLOGY","Score":null,"Total":0}
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。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
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.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
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
期刊最新文献
Assessment of the pattern, severity, and outcomes of acute mood stabilizer drug poisoning. miR-361-3p overexpression promotes apoptosis and inflammation by regulating the USP49/IκBα/NF-κB pathway to aggravate sepsis-induced myocardial injury. Unveiling the interspecies correlation and sensitivity factor analysis of rat and mouse acute oral toxicity of antimicrobial agents: first QSTR and QTTR Modeling report. Stress survival and longevity of Caenorhabditis elegans lacking NCS-1. Lipid-core nanocapsules containing simvastatin do not affect the biochemical and hematological indicators of toxicity in rats.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1