Artesunate demonstrates neuroprotective effect through activation of lysosomal function and inhibition of cGAS-STING pathway

IF 4.6 2区 医学 Q1 NEUROSCIENCES Neuropharmacology Pub Date : 2025-07-01 Epub Date: 2025-03-19 DOI:10.1016/j.neuropharm.2025.110426
Hongqiao Wei , Yongxin Chen , Zhenmin Qin , Honglei Wang , Yujia Liu , Tang Song , Yong Wu , Wanxiang Hu , Xiaowei Huang , Guodong Lu , Jing Zhou
{"title":"Artesunate demonstrates neuroprotective effect through activation of lysosomal function and inhibition of cGAS-STING pathway","authors":"Hongqiao Wei ,&nbsp;Yongxin Chen ,&nbsp;Zhenmin Qin ,&nbsp;Honglei Wang ,&nbsp;Yujia Liu ,&nbsp;Tang Song ,&nbsp;Yong Wu ,&nbsp;Wanxiang Hu ,&nbsp;Xiaowei Huang ,&nbsp;Guodong Lu ,&nbsp;Jing Zhou","doi":"10.1016/j.neuropharm.2025.110426","DOIUrl":null,"url":null,"abstract":"<div><div>Artesunate, a derivative of artemisinin, has a variety of pharmacological effects. Its potential application in ischemic brain injury still largely unknown. This study investigated the therapeutic effect and pharmacological mechanism of artesunate in neuronal injury following cerebral ischemia, and explore the potential role of lysosomal function and cGAS-STING signaling pathway in ischemia injury and artesunate treatment. Studies in rat models have revealed that artesunate can ameliorate neuronal injury and improve learning and memory function following ischemic insults. Furthermore, both <em>in vivo</em> and <em>in vitro</em> studies have confirmed that artesunate can protect neural cells from ischemic injury-induced cell death. Mechanistically, artesunate appears to exert its neuroprotective actions by activating lysosomal function and inhibiting the cGAS-STING pathway-mediated inflammatory response. Our findings provide valuable insights into the therapeutic effects of artesunate exerting a neuroprotective role in chronic ischemic brain injury by activating lysosomal function, inhibiting the cGAS-STING pathway, and regulating the inflammatory response. This study offers a potential therapeutic strategy by regulating lysosome for the treatment of stroke and related neurological disorders.</div></div>","PeriodicalId":19139,"journal":{"name":"Neuropharmacology","volume":"272 ","pages":"Article 110426"},"PeriodicalIF":4.6000,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuropharmacology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0028390825001327","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/3/19 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0

Abstract

Artesunate, a derivative of artemisinin, has a variety of pharmacological effects. Its potential application in ischemic brain injury still largely unknown. This study investigated the therapeutic effect and pharmacological mechanism of artesunate in neuronal injury following cerebral ischemia, and explore the potential role of lysosomal function and cGAS-STING signaling pathway in ischemia injury and artesunate treatment. Studies in rat models have revealed that artesunate can ameliorate neuronal injury and improve learning and memory function following ischemic insults. Furthermore, both in vivo and in vitro studies have confirmed that artesunate can protect neural cells from ischemic injury-induced cell death. Mechanistically, artesunate appears to exert its neuroprotective actions by activating lysosomal function and inhibiting the cGAS-STING pathway-mediated inflammatory response. Our findings provide valuable insights into the therapeutic effects of artesunate exerting a neuroprotective role in chronic ischemic brain injury by activating lysosomal function, inhibiting the cGAS-STING pathway, and regulating the inflammatory response. This study offers a potential therapeutic strategy by regulating lysosome for the treatment of stroke and related neurological disorders.

Abstract Image

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
青蒿琥酯通过激活溶酶体功能和抑制cGAS-STING通路显示神经保护作用。
青蒿琥酯是青蒿素的衍生物,具有多种药理作用。其在缺血性脑损伤中的潜在应用仍是未知的。本研究考察了青蒿琥酯对脑缺血后神经元损伤的治疗作用及药理机制,探讨溶酶体功能及cGAS-STING信号通路在缺血损伤及青蒿琥酯治疗中的潜在作用。大鼠模型研究表明,青蒿琥酯可以改善缺血性损伤后的神经元损伤,改善学习和记忆功能。此外,体内和体外研究证实,青蒿琥酯可以保护神经细胞免受缺血性损伤引起的细胞死亡。机制上,青蒿琥酯似乎通过激活溶酶体功能和抑制cGAS-STING途径介导的炎症反应来发挥其神经保护作用。我们的研究结果为青蒿琥酯通过激活溶酶体功能、抑制cGAS-STING通路和调节炎症反应,在慢性缺血性脑损伤中发挥神经保护作用的治疗效果提供了有价值的见解。本研究提供了一种通过调节溶酶体治疗中风和相关神经系统疾病的潜在治疗策略。
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
文献相关原料
公司名称
产品信息
阿拉丁
Artesunate
来源期刊
Neuropharmacology
Neuropharmacology 医学-神经科学
CiteScore
10.00
自引率
4.30%
发文量
288
审稿时长
45 days
期刊介绍: Neuropharmacology publishes high quality, original research and review articles within the discipline of neuroscience, especially articles with a neuropharmacological component. However, papers within any area of neuroscience will be considered. The journal does not usually accept clinical research, although preclinical neuropharmacological studies in humans may be considered. The journal only considers submissions in which the chemical structures and compositions of experimental agents are readily available in the literature or disclosed by the authors in the submitted manuscript. Only in exceptional circumstances will natural products be considered, and then only if the preparation is well defined by scientific means. Neuropharmacology publishes articles of any length (original research and reviews).
期刊最新文献
Hypocretin receptor 1 blockade early in abstinence reduces future demand for cocaine Cannabidiol reduces the latency for the behavioral effect of escitalopram in chronically stressed male mice: involvement of NAPE-PLD expressed in parvalbumin-positive interneurons and the prefrontal cortex A novel rat model harboring two BDNF gene mutations exhibiting autism-like behaviors and cognitive impairments Dose- and sex-related effects of the MAGL inhibitor MCH11 on binge-like ethanol consumption in mice Running exercise attenuates excitatory synaptic loss in the medial prefrontal cortex of CUS rats: Potential modulation of microglial and astrocytic synaptic contacts
×
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