Exosomes obtained from human adipose-derived stem cells alleviate epileptogenesis in the pentylenetetrazol model of epilepsy.

IF 1.7 4区 医学 Q4 NEUROSCIENCES Neuroreport Pub Date : 2024-12-24 DOI:10.1097/WNR.0000000000002133
Fateme Derisfard, Zahra Jafarinezhad, Negar Azarpira, Mohammad Reza Namavar, Hadi Aligholi
{"title":"Exosomes obtained from human adipose-derived stem cells alleviate epileptogenesis in the pentylenetetrazol model of epilepsy.","authors":"Fateme Derisfard, Zahra Jafarinezhad, Negar Azarpira, Mohammad Reza Namavar, Hadi Aligholi","doi":"10.1097/WNR.0000000000002133","DOIUrl":null,"url":null,"abstract":"<p><p>As exosome therapy is a promising treatment in neurological disorders including epilepsy, the present study aimed to evaluate the effects of exosomes obtained from human adipose-derived stem cells (ADSCs) on pentylenetetrazol (PTZ) model of epilepsy in mice. Thirty adult mice were divided into PTZ, diazepam + PTZ, and exosome (5, 10, and 15 µg) + PTZ groups. The exosomes were administered intranasally 30 min before PTZ injection. The seizure latency, tonic-clonic onset, seizure duration, and mortality protection rate were monitored. Also, the level of hippocampal malondialdehyde (MDA), the oxidative stress marker, was evaluated. Exosomes in 5 and 15 µg concentration significantly increased seizure latency. Only 15 µg of exosomes induced a considerable delay in tonic-clonic onset. Seizure duration was significantly attenuated in the 5 µg exosome group. In addition, the 5-µg exosome indicated the highest mortality protection rate. Furthermore, the MDA level was significantly reduced in all animals treated by exosomes. Exosomes obtained from human ADSCs could alleviate epileptogenesis induced by PTZ maybe through reducing hippocampal oxidative stress.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":""},"PeriodicalIF":1.7000,"publicationDate":"2024-12-24","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.0000000000002133","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

As exosome therapy is a promising treatment in neurological disorders including epilepsy, the present study aimed to evaluate the effects of exosomes obtained from human adipose-derived stem cells (ADSCs) on pentylenetetrazol (PTZ) model of epilepsy in mice. Thirty adult mice were divided into PTZ, diazepam + PTZ, and exosome (5, 10, and 15 µg) + PTZ groups. The exosomes were administered intranasally 30 min before PTZ injection. The seizure latency, tonic-clonic onset, seizure duration, and mortality protection rate were monitored. Also, the level of hippocampal malondialdehyde (MDA), the oxidative stress marker, was evaluated. Exosomes in 5 and 15 µg concentration significantly increased seizure latency. Only 15 µg of exosomes induced a considerable delay in tonic-clonic onset. Seizure duration was significantly attenuated in the 5 µg exosome group. In addition, the 5-µg exosome indicated the highest mortality protection rate. Furthermore, the MDA level was significantly reduced in all animals treated by exosomes. Exosomes obtained from human ADSCs could alleviate epileptogenesis induced by PTZ maybe through reducing hippocampal oxidative stress.

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
从人脂肪来源的干细胞中获得的外泌体减轻戊四氮唑癫痫模型的癫痫发生。
鉴于外泌体疗法在包括癫痫在内的神经系统疾病中是一种很有前景的治疗方法,本研究旨在评估从人脂肪源性干细胞(ADSCs)中获得的外泌体对小鼠戊四氮唑(PTZ)癫痫模型的影响。将30只成年小鼠分为PTZ、地西泮+ PTZ和外泌体(5、10和15µg) + PTZ组。外泌体在PTZ注射前30分钟经鼻给药。监测发作潜伏期、强直阵挛发作、发作持续时间和死亡率保护率。此外,我们还评估了氧化应激标志物海马丙二醛(MDA)的水平。5µg和15µg浓度的外泌体显著增加癫痫发作潜伏期。仅15µg外泌体可显著延缓强直-阵挛发作。5µg外泌体组癫痫发作时间明显缩短。此外,5µg外泌体显示出最高的死亡保护率。此外,外泌体处理的所有动物的MDA水平均显著降低。从人ADSCs中获得的外泌体可能通过降低海马氧化应激来减轻PTZ诱导的癫痫发生。
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
Aloe-emodin attenuated Aβ-induced tau phosphorylation by autophagy-NLRP3 inflammasome pathway. Protective effects of vitamin D supplementation combined with exercise on depressive-like behaviors in chronic stress rats. Comparative study of behavior and pathology in three mouse models of kainic acid-induced epilepsy. Bone hypertrophy and reduced quality after nucleus pulposus aspiration induces low back pain-like behavior and neuronal hyperexcitability. Celastrol exerts a neuroprotective effect by inhibiting necroptosis and inflammation in intracerebral hemorrhage-induced brain injury.
×
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:604180095
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