Shikonin alleviates asthma phenotypes in mice via an airway epithelial STAT3-dependent mechanism.

IF 1.7 4区 医学 Q2 MEDICINE, GENERAL & INTERNAL
Open Medicine Pub Date : 2024-10-21 eCollection Date: 2024-01-01 DOI:10.1515/med-2024-1016
Yao Zhang, Lizhan Chen, Haifeng Ouyang
{"title":"Shikonin alleviates asthma phenotypes in mice via an airway epithelial STAT3-dependent mechanism.","authors":"Yao Zhang, Lizhan Chen, Haifeng Ouyang","doi":"10.1515/med-2024-1016","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Asthma is an inflammatory disease where the balance between Th1/Th2 and Th17/Treg plays a crucial role in its pathogenesis. Shikonin is used to treat a variety of autoimmune diseases due to its good anti-inflammatory activity. However, the effect and mechanism of shikonin on asthma remain unknown.</p><p><strong>Method: </strong>Mice were sensitized with ovalbumin (OVA)/house dust mite (HDM) and treated with shikonin. Lung inflammation was assessed histologically and via flow cytometry. Bronchoalveolar lavage fluid (BALF) was analyzed for cell counts and cytokines. Shikonin's impact on p-STAT3 was studied <i>in vivo</i> and <i>in vitro.</i></p><p><strong>Results: </strong>Shikonin inhibited OVA or HDM-induced inflammation and airway hyperresponsiveness. Upon treatment, a restoration of the Th1/Th2 and Th17/Treg balance was observed, evidenced by a reduction in IL-4 and IL-17A levels in BALF, alongside an elevation in interferon-gamma and IL-10. Furthermore, shikonin impeded the infiltration of eosinophils, neutrophils, macrophages, and lymphocytes into lung tissue. The observed decrease in STAT3 phosphorylation and diminished nuclear translocation of p-STAT3 confirmed that shikonin promotes the balance of Th1/Th2 and Th17/Treg by regulating airway epithelial STAT3.</p><p><strong>Conclusion: </strong>Shikonin mitigates asthma symptoms through a STAT3-dependent mechanism, indicating its potential as an anti-asthmatic therapeutic agent.</p>","PeriodicalId":19715,"journal":{"name":"Open Medicine","volume":"19 1","pages":"20241016"},"PeriodicalIF":1.7000,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11497215/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Open Medicine","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1515/med-2024-1016","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Asthma is an inflammatory disease where the balance between Th1/Th2 and Th17/Treg plays a crucial role in its pathogenesis. Shikonin is used to treat a variety of autoimmune diseases due to its good anti-inflammatory activity. However, the effect and mechanism of shikonin on asthma remain unknown.

Method: Mice were sensitized with ovalbumin (OVA)/house dust mite (HDM) and treated with shikonin. Lung inflammation was assessed histologically and via flow cytometry. Bronchoalveolar lavage fluid (BALF) was analyzed for cell counts and cytokines. Shikonin's impact on p-STAT3 was studied in vivo and in vitro.

Results: Shikonin inhibited OVA or HDM-induced inflammation and airway hyperresponsiveness. Upon treatment, a restoration of the Th1/Th2 and Th17/Treg balance was observed, evidenced by a reduction in IL-4 and IL-17A levels in BALF, alongside an elevation in interferon-gamma and IL-10. Furthermore, shikonin impeded the infiltration of eosinophils, neutrophils, macrophages, and lymphocytes into lung tissue. The observed decrease in STAT3 phosphorylation and diminished nuclear translocation of p-STAT3 confirmed that shikonin promotes the balance of Th1/Th2 and Th17/Treg by regulating airway epithelial STAT3.

Conclusion: Shikonin mitigates asthma symptoms through a STAT3-dependent mechanism, indicating its potential as an anti-asthmatic therapeutic agent.

志贺宁通过气道上皮 STAT3 依赖性机制缓解小鼠的哮喘表型
背景:哮喘是一种炎症性疾病,Th1/Th2 和 Th17/Treg 之间的平衡在其发病机制中起着至关重要的作用。志贺宁具有良好的抗炎活性,可用于治疗多种自身免疫性疾病。然而,志贺宁对哮喘的作用和机制仍不清楚:方法:用卵清蛋白(OVA)/屋尘螨(HDM)致敏小鼠,并用志贺宁治疗。通过组织学和流式细胞术评估肺部炎症。对支气管肺泡灌洗液(BALF)进行了细胞计数和细胞因子分析。研究了 Shikonin 在体内和体外对 p-STAT3 的影响:结果:Shikonin 可抑制 OVA 或 HDM 诱导的炎症和气道高反应性。治疗后,Th1/Th2和Th17/Treg平衡得到恢复,这体现在BALF中IL-4和IL-17A水平的降低,以及γ干扰素和IL-10水平的升高。此外,志贺宁还能抑制嗜酸性粒细胞、中性粒细胞、巨噬细胞和淋巴细胞向肺组织的浸润。观察到的 STAT3 磷酸化下降和 p-STAT3 核转位减少证实,志贺宁通过调节气道上皮 STAT3 促进 Th1/Th2 和 Th17/Treg 的平衡:结论:志贺宁通过 STAT3 依赖性机制减轻哮喘症状,显示了其作为抗哮喘治疗药物的潜力。
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 求助全文
来源期刊
Open Medicine
Open Medicine Medicine-General Medicine
CiteScore
3.00
自引率
0.00%
发文量
153
审稿时长
20 weeks
期刊介绍: Open Medicine is an open access journal that provides users with free, instant, and continued access to all content worldwide. The primary goal of the journal has always been a focus on maintaining the high quality of its published content. Its mission is to facilitate the exchange of ideas between medical science researchers from different countries. Papers connected to all fields of medicine and public health are welcomed. Open Medicine accepts submissions of research articles, reviews, case reports, letters to editor and book reviews.
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信