通过加速脑组织间液的排泄来预防缺血性中风的新型神经保护方法。

IF 8 2区 生物学 Q1 BIOLOGY Science China Life Sciences Pub Date : 2024-10-01 Epub Date: 2024-08-02 DOI:10.1007/s11427-024-2592-4
Jingge Lian, Liu Yang, Hanbo Tan, Shaoyi Su, Leonor Serrano Lopes, Fangxiao Cheng, Junhao Yan, Yu Fu, Wanyi Fu, Zhaoheng Xie, Jianfei Sun, Jicong Zhang, Zhiqian Tong, Yajuan Gao, Hongbin Han
{"title":"通过加速脑组织间液的排泄来预防缺血性中风的新型神经保护方法。","authors":"Jingge Lian, Liu Yang, Hanbo Tan, Shaoyi Su, Leonor Serrano Lopes, Fangxiao Cheng, Junhao Yan, Yu Fu, Wanyi Fu, Zhaoheng Xie, Jianfei Sun, Jicong Zhang, Zhiqian Tong, Yajuan Gao, Hongbin Han","doi":"10.1007/s11427-024-2592-4","DOIUrl":null,"url":null,"abstract":"<p><p>Ischemic stroke is a leading cause of death and disability worldwide. Inflammatory response after stroke determines the outcome of ischemic injury. A recent study has reported an efficient method, epidural arterial implantation (EAI), for accelerating interstitial fluid (ISF) drainage, which provides a promising strategy to clear pro-inflammatory cytokines in the brain extracellular space (ECS). In this study, the method of EAI was modified (m-EAI) to control its function of accelerating the ISF drainage at different time points following ischemic attack. The neuroprotective effect of m-EAI on ischemic stroke was evaluated with the transient middle cerebral artery occlusion (tMCAO) rat model. The results demonstrated the accumulation of IL-1β, IL-6, and TNF-α was significantly decreased by activating m-EAI at 7 d before and immediately after ischemic attack in tMCAO rats, accompanied with decreased infarct volume and improved neurological function. This study consolidates the hypothesis of exacerbated ischemic damage by inflammatory response and provides a new perspective to treat encephalopathy via brain ECS. Further research is essential to investigate whether m-EAI combined with neuroprotective drugs could enhance the therapeutic effect on ischemic stroke.</p>","PeriodicalId":21576,"journal":{"name":"Science China Life Sciences","volume":" ","pages":"2213-2223"},"PeriodicalIF":8.0000,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"A novel neuroprotective method against ischemic stroke by accelerating the drainage of brain interstitial fluid.\",\"authors\":\"Jingge Lian, Liu Yang, Hanbo Tan, Shaoyi Su, Leonor Serrano Lopes, Fangxiao Cheng, Junhao Yan, Yu Fu, Wanyi Fu, Zhaoheng Xie, Jianfei Sun, Jicong Zhang, Zhiqian Tong, Yajuan Gao, Hongbin Han\",\"doi\":\"10.1007/s11427-024-2592-4\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Ischemic stroke is a leading cause of death and disability worldwide. Inflammatory response after stroke determines the outcome of ischemic injury. A recent study has reported an efficient method, epidural arterial implantation (EAI), for accelerating interstitial fluid (ISF) drainage, which provides a promising strategy to clear pro-inflammatory cytokines in the brain extracellular space (ECS). In this study, the method of EAI was modified (m-EAI) to control its function of accelerating the ISF drainage at different time points following ischemic attack. The neuroprotective effect of m-EAI on ischemic stroke was evaluated with the transient middle cerebral artery occlusion (tMCAO) rat model. The results demonstrated the accumulation of IL-1β, IL-6, and TNF-α was significantly decreased by activating m-EAI at 7 d before and immediately after ischemic attack in tMCAO rats, accompanied with decreased infarct volume and improved neurological function. This study consolidates the hypothesis of exacerbated ischemic damage by inflammatory response and provides a new perspective to treat encephalopathy via brain ECS. Further research is essential to investigate whether m-EAI combined with neuroprotective drugs could enhance the therapeutic effect on ischemic stroke.</p>\",\"PeriodicalId\":21576,\"journal\":{\"name\":\"Science China Life Sciences\",\"volume\":\" \",\"pages\":\"2213-2223\"},\"PeriodicalIF\":8.0000,\"publicationDate\":\"2024-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Science China Life Sciences\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1007/s11427-024-2592-4\",\"RegionNum\":2,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/8/2 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Science China Life Sciences","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s11427-024-2592-4","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/8/2 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"BIOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

缺血性中风是全球死亡和残疾的主要原因。中风后的炎症反应决定了缺血性损伤的结局。最近的一项研究报道了一种有效的方法,即硬膜外动脉植入术(EAI),用于加速间质液体(ISF)的引流,为清除脑细胞外空间(ECS)中的促炎细胞因子提供了一种有前途的策略。本研究对 EAI 方法进行了改进(m-EAI),以控制其在缺血发作后不同时间点加速 ISF 引流的功能。研究人员利用短暂性大脑中动脉闭塞(tMCAO)大鼠模型评估了 m-EAI 对缺血性脑卒中的神经保护作用。结果表明,在缺血发作前 7 d 和紧接着缺血发作后 7 d 激活 m-EAI,tMCAO 大鼠体内 IL-1β、IL-6 和 TNF-α 的积累明显减少,同时梗死体积缩小,神经功能得到改善。这项研究巩固了炎症反应加重缺血损伤的假说,为通过脑ECS治疗脑病提供了新的视角。进一步研究 m-EAI 与神经保护药物的结合是否能增强对缺血性脑卒中的治疗效果至关重要。
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
A novel neuroprotective method against ischemic stroke by accelerating the drainage of brain interstitial fluid.

Ischemic stroke is a leading cause of death and disability worldwide. Inflammatory response after stroke determines the outcome of ischemic injury. A recent study has reported an efficient method, epidural arterial implantation (EAI), for accelerating interstitial fluid (ISF) drainage, which provides a promising strategy to clear pro-inflammatory cytokines in the brain extracellular space (ECS). In this study, the method of EAI was modified (m-EAI) to control its function of accelerating the ISF drainage at different time points following ischemic attack. The neuroprotective effect of m-EAI on ischemic stroke was evaluated with the transient middle cerebral artery occlusion (tMCAO) rat model. The results demonstrated the accumulation of IL-1β, IL-6, and TNF-α was significantly decreased by activating m-EAI at 7 d before and immediately after ischemic attack in tMCAO rats, accompanied with decreased infarct volume and improved neurological function. This study consolidates the hypothesis of exacerbated ischemic damage by inflammatory response and provides a new perspective to treat encephalopathy via brain ECS. Further research is essential to investigate whether m-EAI combined with neuroprotective drugs could enhance the therapeutic effect on ischemic stroke.

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
CiteScore
15.10
自引率
8.80%
发文量
2907
审稿时长
3.2 months
期刊介绍: Science China Life Sciences is a scholarly journal co-sponsored by the Chinese Academy of Sciences and the National Natural Science Foundation of China, and it is published by Science China Press. The journal is dedicated to publishing high-quality, original research findings in both basic and applied life science research.
期刊最新文献
Exaptation of pectoral fins for olfaction in the spiny red gurnard (Chelidonichthys spinosus) through an ancient receptor. Genomic analysis of modern maize inbred lines reveals diversity and selective breeding effects. Genome editing technology and medical applications. Dual activation of soybean resistance against Phytophthora sojae by pectin lyase and degraded pectin oligosaccharides. Selenium metabolism and selenoproteins function in brain and encephalopathy.
×
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