Quercetin regulates dendritic cell activation by targeting STAT4 in the treatment of experimental autoimmune encephalomyelitis

IF 3.4 3区 医学 Q2 PHARMACOLOGY & PHARMACY Toxicology and applied pharmacology Pub Date : 2024-07-01 Epub Date: 2024-05-31 DOI:10.1016/j.taap.2024.116980
Fang Zhou , Yu-Xin Guo , Rui Gao , Xiao-Yu Ji , Yu-Xuan Tang , Li-Bin Wang , Yuan Zhang , Xing Li
{"title":"Quercetin regulates dendritic cell activation by targeting STAT4 in the treatment of experimental autoimmune encephalomyelitis","authors":"Fang Zhou ,&nbsp;Yu-Xin Guo ,&nbsp;Rui Gao ,&nbsp;Xiao-Yu Ji ,&nbsp;Yu-Xuan Tang ,&nbsp;Li-Bin Wang ,&nbsp;Yuan Zhang ,&nbsp;Xing Li","doi":"10.1016/j.taap.2024.116980","DOIUrl":null,"url":null,"abstract":"<div><p>Multiple sclerosis (MS) is a class of autoimmune diseases mainly caused by the immune system attacking the myelin sheath of the axons in the nervous system. Although the pathogenesis of MS is complex, studies have shown that dendritic cells (DCs) play a vital role in the pathogenesis of MS. Quercetin (QU) has a unique advantage in clinical application, especially for treating autoimmune diseases. However, the mechanism of QU in the treatment of experimental autoimmune encephalomyelitis (EAE) remains unclear. In this study, we explore the potential role of QU in EAE. Finally, we find that QU has anti-inflammatory activities and neural protective effects in EAE. The experimental results suggest that the cellular basis for QU's function is to inhibit the activation of DCs while modulating the Th17 cell differentiation in the co-culture system. Further, QU may target STAT4 to inhibit its activation in DCs. This work will be of great significance for the future development and utilization of QU.</p></div>","PeriodicalId":23174,"journal":{"name":"Toxicology and applied pharmacology","volume":"488 ","pages":"Article 116980"},"PeriodicalIF":3.4000,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Toxicology and applied pharmacology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0041008X24001789","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/5/31 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"PHARMACOLOGY & PHARMACY","Score":null,"Total":0}
引用次数: 0

Abstract

Multiple sclerosis (MS) is a class of autoimmune diseases mainly caused by the immune system attacking the myelin sheath of the axons in the nervous system. Although the pathogenesis of MS is complex, studies have shown that dendritic cells (DCs) play a vital role in the pathogenesis of MS. Quercetin (QU) has a unique advantage in clinical application, especially for treating autoimmune diseases. However, the mechanism of QU in the treatment of experimental autoimmune encephalomyelitis (EAE) remains unclear. In this study, we explore the potential role of QU in EAE. Finally, we find that QU has anti-inflammatory activities and neural protective effects in EAE. The experimental results suggest that the cellular basis for QU's function is to inhibit the activation of DCs while modulating the Th17 cell differentiation in the co-culture system. Further, QU may target STAT4 to inhibit its activation in DCs. This work will be of great significance for the future development and utilization of QU.

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
槲皮素在治疗实验性自身免疫性脑脊髓炎中通过靶向 STAT4 调节树突状细胞活化
多发性硬化症(MS)是一类自身免疫性疾病,主要由免疫系统攻击神经系统轴突的髓鞘引起。虽然多发性硬化症的发病机制十分复杂,但研究表明,树突状细胞(DCs)在多发性硬化症的发病机制中起着至关重要的作用。槲皮素(QU)在临床应用中具有独特的优势,尤其是在治疗自身免疫性疾病方面。然而,槲皮素治疗实验性自身免疫性脑脊髓炎(EAE)的机制仍不清楚。在本研究中,我们探讨了 QU 在 EAE 中的潜在作用。最后,我们发现 QU 在 EAE 中具有抗炎活性和神经保护作用。实验结果表明,QU 发挥作用的细胞基础是抑制 DCs 的活化,同时调节共培养系统中 Th17 细胞的分化。此外,QU可能以STAT4为靶点,抑制其在DCs中的激活。这项工作对 QU 未来的开发和利用具有重要意义。
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
CiteScore
6.80
自引率
2.60%
发文量
309
审稿时长
32 days
期刊介绍: Toxicology and Applied Pharmacology publishes original scientific research of relevance to animals or humans pertaining to the action of chemicals, drugs, or chemically-defined natural products. Regular articles address mechanistic approaches to physiological, pharmacologic, biochemical, cellular, or molecular understanding of toxicologic/pathologic lesions and to methods used to describe these responses. Safety Science articles address outstanding state-of-the-art preclinical and human translational characterization of drug and chemical safety employing cutting-edge science. Highly significant Regulatory Safety Science articles will also be considered in this category. Papers concerned with alternatives to the use of experimental animals are encouraged. Short articles report on high impact studies of broad interest to readers of TAAP that would benefit from rapid publication. These articles should contain no more than a combined total of four figures and tables. Authors should include in their cover letter the justification for consideration of their manuscript as a short article.
期刊最新文献
Dexmedetomidine regulates fatty acid oxidation through the AMPK/PGC-1α/CPT1A pathway to mitigate renal ischaemia-reperfusion injury RUNDC3A-AS1 is an adverse prognostic factor for triple-negative breast cancer which mediates the Warburg effect and Adriamycin resistance by targeting miR-224-3p/COL5A2 Aloperine alleviates lung ischemia-reperfusion injury by modulating ferroptosis via the STAT-1 pathway Clarification on the interpretation of TCGA-SARC data in the prognostic evaluation of MMP13 in osteosarcoma MiR-29a/DNMT3A axis participates in Dihydroartemisinin's suppression on lung adenocarcinoma: Implications for overcoming acquired resistance to EGFR-TKIs
×
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