The involvement of lidocaine in amyloid-β1-42-dependent mitochondrial dysfunction and apoptosis in hippocampal neurons via nerve growth factor-protein kinase B pathway.

IF 1.6 4区 医学 Q4 NEUROSCIENCES Neuroreport Pub Date : 2024-12-11 Epub Date: 2024-10-22 DOI:10.1097/WNR.0000000000002105
Jianlian Guo, Yong Xu, Jie Liu, Xueqi Hou
{"title":"The involvement of lidocaine in amyloid-β1-42-dependent mitochondrial dysfunction and apoptosis in hippocampal neurons via nerve growth factor-protein kinase B pathway.","authors":"Jianlian Guo, Yong Xu, Jie Liu, Xueqi Hou","doi":"10.1097/WNR.0000000000002105","DOIUrl":null,"url":null,"abstract":"<p><p>This project is conceived to reveal the role of lidocaine in the process of Alzheimer's disease (AD) and its possible downstream targets. After the employment of AD cell model in mice hippocampal neuronal HT-22 cells in the presence of amyloid-β1-42 (Aβ1-42), Cell Counting Kit-8 method investigated cell viability. Oxidative damage was assayed based on a dichloro-dihydro-fluorescein diacetate fluorescent probe and commercially available kits. The 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbocyanine iodide fluorescent probe estimated mitochondrial function. Terminal-deoxynucleotidyl transferase mediated nick end labeling, western blotting, and immunofluorescence appraised the apoptotic level. Western blot also ascertained the alternations of nerve growth factors (NGF)-protein kinase B (Akt) pathway-related proteins. Aβ1-42 concentration dependently triggered the viability loss, oxidative damage, and apoptosis in HT-22 cells. Lidocaine promoted the viability and reduced the mitochondrial impairment and mitochondria-dependent apoptosis in Aβ1-42-treated HT-22 cells in a concentration-dependent manner. Besides, lidocaine activated the NGF-Akt pathway and NGF absence blocked NGF-Akt pathway, aggravated mitochondrial dysfunction as well as mitochondria-dependent apoptosis in lidocaine-administrated HT-22 cells in response to Aβ1-42. Altogether, these observations concluded that lidocaine might stimulate NGF-Akt pathway to confer protection against mitochondrial impairment and apoptosis in Aβ1-42-mediated cellular model of AD.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":null,"pages":null},"PeriodicalIF":1.6000,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroreport","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1097/WNR.0000000000002105","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/22 0:00:00","PubModel":"Epub","JCR":"Q4","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

This project is conceived to reveal the role of lidocaine in the process of Alzheimer's disease (AD) and its possible downstream targets. After the employment of AD cell model in mice hippocampal neuronal HT-22 cells in the presence of amyloid-β1-42 (Aβ1-42), Cell Counting Kit-8 method investigated cell viability. Oxidative damage was assayed based on a dichloro-dihydro-fluorescein diacetate fluorescent probe and commercially available kits. The 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbocyanine iodide fluorescent probe estimated mitochondrial function. Terminal-deoxynucleotidyl transferase mediated nick end labeling, western blotting, and immunofluorescence appraised the apoptotic level. Western blot also ascertained the alternations of nerve growth factors (NGF)-protein kinase B (Akt) pathway-related proteins. Aβ1-42 concentration dependently triggered the viability loss, oxidative damage, and apoptosis in HT-22 cells. Lidocaine promoted the viability and reduced the mitochondrial impairment and mitochondria-dependent apoptosis in Aβ1-42-treated HT-22 cells in a concentration-dependent manner. Besides, lidocaine activated the NGF-Akt pathway and NGF absence blocked NGF-Akt pathway, aggravated mitochondrial dysfunction as well as mitochondria-dependent apoptosis in lidocaine-administrated HT-22 cells in response to Aβ1-42. Altogether, these observations concluded that lidocaine might stimulate NGF-Akt pathway to confer protection against mitochondrial impairment and apoptosis in Aβ1-42-mediated cellular model of AD.

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
利多卡因通过神经生长因子-蛋白激酶B通路参与淀粉样β1-42依赖性线粒体功能障碍和海马神经元凋亡的研究
本项目旨在揭示利多卡因在阿尔茨海默病(AD)过程中的作用及其可能的下游靶点。在淀粉样蛋白-β1-42(Aβ1-42)存在的情况下,利用小鼠海马神经元 HT-22 细胞的 AD 细胞模型,采用细胞计数工具包-8 法检测细胞活力。利用二氯二氢荧光素二乙酸酯荧光探针和市售试剂盒检测氧化损伤。5,5',6,6'-四氯-1,1',3,3'-四乙基苯并咪唑羰花青碘化物荧光探针可评估线粒体功能。末端脱氧核苷酸转移酶介导的缺口标记、Western 印迹和免疫荧光评估了细胞凋亡水平。Western 印迹还检测了神经生长因子(NGF)-蛋白激酶 B(Akt)通路相关蛋白的变化。Aβ1-42浓度依赖性地引发HT-22细胞活力下降、氧化损伤和凋亡。利多卡因促进了Aβ1-42处理的HT-22细胞的活力,并减少了线粒体损伤和线粒体依赖性凋亡,其作用呈浓度依赖性。此外,利多卡因激活了NGF-Akt通路,而NGF的缺失阻断了NGF-Akt通路,加重了利多卡因给药的HT-22细胞在Aβ1-42作用下的线粒体功能障碍和线粒体依赖性凋亡。总之,这些观察结果表明,利多卡因可刺激NGF-Akt通路,从而在Aβ1-42-介导的AD细胞模型中保护细胞免受线粒体损伤和凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Neuroreport
Neuroreport 医学-神经科学
CiteScore
3.20
自引率
0.00%
发文量
150
审稿时长
1 months
期刊介绍: NeuroReport is a channel for rapid communication of new findings in neuroscience. It is a forum for the publication of short but complete reports of important studies that require very fast publication. Papers are accepted on the basis of the novelty of their finding, on their significance for neuroscience and on a clear need for rapid publication. Preliminary communications are not suitable for the Journal. Submitted articles undergo a preliminary review by the editor. Some articles may be returned to authors without further consideration. Those being considered for publication will undergo further assessment and peer-review by the editors and those invited to do so from a reviewer pool. The core interest of the Journal is on studies that cast light on how the brain (and the whole of the nervous system) works. We aim to give authors a decision on their submission within 2-5 weeks, and all accepted articles appear in the next issue to press.
期刊最新文献
Different dorsolateral prefrontal activation during an emotionalautobiographical memory task between male and female depressed individuals: a fNIRS study. Reduced glutathione attenuates pediatric sepsis-associated encephalopathy by inhibiting inflammatory cytokine release and mitigating lipid peroxidation-induced brain injury. The involvement of lidocaine in amyloid-β1-42-dependent mitochondrial dysfunction and apoptosis in hippocampal neurons via nerve growth factor-protein kinase B pathway. Topological organization of the brain network in thyroid-associated ophthalmopathy using graph theoretical analysis. Disrupted functional connectivity of bilateral nucleus accumbens in major depressive disorder with and without melancholic features.
×
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