青黛(天然靛蓝)通过调节 AHR-Th17/Treg 通路促进溃疡性结肠炎粘膜愈合和症状改善的临床、药理和体内研究。

IF 4.4 3区 医学 Q2 IMMUNOLOGY Journal of Inflammation-London Pub Date : 2024-11-05 DOI:10.1186/s12950-024-00413-x
Sizhen Gu, Yan Xue, Xiaowen Liu, Yini Tang, Dong Wang, Dongmei Wu, Mingrong Yao, Zehua Xia, Sen Yang, Gan Cai, Shigui Xue, Danbo Dou
{"title":"青黛(天然靛蓝)通过调节 AHR-Th17/Treg 通路促进溃疡性结肠炎粘膜愈合和症状改善的临床、药理和体内研究。","authors":"Sizhen Gu, Yan Xue, Xiaowen Liu, Yini Tang, Dong Wang, Dongmei Wu, Mingrong Yao, Zehua Xia, Sen Yang, Gan Cai, Shigui Xue, Danbo Dou","doi":"10.1186/s12950-024-00413-x","DOIUrl":null,"url":null,"abstract":"<p><p>Qingdai (QD), derived from various plant sources, is commonly used in traditional Chinese medicine for ulcerative colitis (UC) treatment. However, the clinical efficacy and mechanisms of orally administered QD remain unclear. This study aims to evaluate QD's efficacy in UC treatment and uncover its active components and mechanisms. A randomized controlled trial compared QD to Adisa, followed by UPLC-Q-TOF/MS and network pharmacology analyses to identify QD's core components and targets. In vivo experiments on a UC mouse model explored QD's impact on the AHR-Th17/Treg pathway using PCR, WB, ELISA, and flow cytometry. Results showed QD's efficacy in UC treatment, with mucosal healing and remission comparable to Adisa. UPLC-Q-TOF/MS identified 16 core components in mouse colon tissue, with network pharmacology revealing 67 targets, potentially involving the IL-17 signaling pathway and Th17 cell differentiation. QD and its components up-regulated AHR, CYP1A1, and Foxp3, while down-regulating RORγt. Additionally, QD modulated pro-inflammatory (IL-6, IL-17 A) and anti-inflammatory (IL-10, TGF-β1) factors, and Treg/Th17 cell ratios in LPMC. Oral QD administration effectively promoted mucosal healing and improved UC symptoms, potentially through AHR-Th17/Treg pathway regulation.</p>","PeriodicalId":56120,"journal":{"name":"Journal of Inflammation-London","volume":null,"pages":null},"PeriodicalIF":4.4000,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11536804/pdf/","citationCount":"0","resultStr":"{\"title\":\"Clinical, pharmacology and in vivo studies of QingDai (indigo naturalis) promotes mucosal healing and symptom improvement in ulcerative colitis by regulating the AHR-Th17/Treg pathway.\",\"authors\":\"Sizhen Gu, Yan Xue, Xiaowen Liu, Yini Tang, Dong Wang, Dongmei Wu, Mingrong Yao, Zehua Xia, Sen Yang, Gan Cai, Shigui Xue, Danbo Dou\",\"doi\":\"10.1186/s12950-024-00413-x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Qingdai (QD), derived from various plant sources, is commonly used in traditional Chinese medicine for ulcerative colitis (UC) treatment. However, the clinical efficacy and mechanisms of orally administered QD remain unclear. This study aims to evaluate QD's efficacy in UC treatment and uncover its active components and mechanisms. A randomized controlled trial compared QD to Adisa, followed by UPLC-Q-TOF/MS and network pharmacology analyses to identify QD's core components and targets. In vivo experiments on a UC mouse model explored QD's impact on the AHR-Th17/Treg pathway using PCR, WB, ELISA, and flow cytometry. Results showed QD's efficacy in UC treatment, with mucosal healing and remission comparable to Adisa. UPLC-Q-TOF/MS identified 16 core components in mouse colon tissue, with network pharmacology revealing 67 targets, potentially involving the IL-17 signaling pathway and Th17 cell differentiation. QD and its components up-regulated AHR, CYP1A1, and Foxp3, while down-regulating RORγt. Additionally, QD modulated pro-inflammatory (IL-6, IL-17 A) and anti-inflammatory (IL-10, TGF-β1) factors, and Treg/Th17 cell ratios in LPMC. Oral QD administration effectively promoted mucosal healing and improved UC symptoms, potentially through AHR-Th17/Treg pathway regulation.</p>\",\"PeriodicalId\":56120,\"journal\":{\"name\":\"Journal of Inflammation-London\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":4.4000,\"publicationDate\":\"2024-11-05\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11536804/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Inflammation-London\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1186/s12950-024-00413-x\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"IMMUNOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Inflammation-London","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s12950-024-00413-x","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

清瘟散(QD)提取自多种植物,是治疗溃疡性结肠炎(UC)的常用中药。然而,口服青黛的临床疗效和机制仍不清楚。本研究旨在评估芪冬片治疗溃疡性结肠炎的疗效,并揭示其活性成分和机制。随机对照试验比较了 QD 和 Adisa,随后通过 UPLC-Q-TOF/MS 和网络药理学分析确定了 QD 的核心成分和靶点。在 UC 小鼠模型上进行的体内实验使用 PCR、WB、ELISA 和流式细胞术探讨了 QD 对 AHR-Th17/Treg 通路的影响。结果表明,QD 对治疗 UC 具有疗效,粘膜愈合和缓解效果与 Adisa 相当。UPLC-Q-TOF/MS 在小鼠结肠组织中发现了 16 种核心成分,网络药理学发现了 67 个靶点,可能涉及 IL-17 信号通路和 Th17 细胞分化。QD及其成分能上调AHR、CYP1A1和Foxp3,同时下调RORγt。此外,QD还能调节LPMC中的促炎因子(IL-6、IL-17 A)和抗炎因子(IL-10、TGF-β1)以及Treg/Th17细胞比例。口服QD可有效促进粘膜愈合并改善UC症状,这可能是通过AHR-Th17/Treg通路调节实现的。
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
Clinical, pharmacology and in vivo studies of QingDai (indigo naturalis) promotes mucosal healing and symptom improvement in ulcerative colitis by regulating the AHR-Th17/Treg pathway.

Qingdai (QD), derived from various plant sources, is commonly used in traditional Chinese medicine for ulcerative colitis (UC) treatment. However, the clinical efficacy and mechanisms of orally administered QD remain unclear. This study aims to evaluate QD's efficacy in UC treatment and uncover its active components and mechanisms. A randomized controlled trial compared QD to Adisa, followed by UPLC-Q-TOF/MS and network pharmacology analyses to identify QD's core components and targets. In vivo experiments on a UC mouse model explored QD's impact on the AHR-Th17/Treg pathway using PCR, WB, ELISA, and flow cytometry. Results showed QD's efficacy in UC treatment, with mucosal healing and remission comparable to Adisa. UPLC-Q-TOF/MS identified 16 core components in mouse colon tissue, with network pharmacology revealing 67 targets, potentially involving the IL-17 signaling pathway and Th17 cell differentiation. QD and its components up-regulated AHR, CYP1A1, and Foxp3, while down-regulating RORγt. Additionally, QD modulated pro-inflammatory (IL-6, IL-17 A) and anti-inflammatory (IL-10, TGF-β1) factors, and Treg/Th17 cell ratios in LPMC. Oral QD administration effectively promoted mucosal healing and improved UC symptoms, potentially through AHR-Th17/Treg pathway regulation.

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
7.90
自引率
0.00%
发文量
18
审稿时长
>12 weeks
期刊介绍: Journal of Inflammation welcomes research submissions on all aspects of inflammation. The five classical symptoms of inflammation, namely redness (rubor), swelling (tumour), heat (calor), pain (dolor) and loss of function (functio laesa), are only part of the story. The term inflammation is taken to include the full range of underlying cellular and molecular mechanisms involved, not only in the production of the inflammatory responses but, more importantly in clinical terms, in the healing process as well. Thus the journal covers molecular, cellular, animal and clinical studies, and related aspects of pharmacology, such as anti-inflammatory drug development, trials and therapeutic developments. It also considers publication of negative findings. Journal of Inflammation aims to become the leading online journal on inflammation and, as online journals replace printed ones over the next decade, the main open access inflammation journal. Open access guarantees a larger audience, and thus impact, than any restricted access equivalent, and increasingly so, as the escalating costs of printed journals puts them outside University budgets. The unrestricted access to research findings in inflammation aids in promoting dynamic and productive dialogue between industrial and academic members of the inflammation research community, which plays such an important part in the development of future generations of anti-inflammatory therapies.
期刊最新文献
Clinical, pharmacology and in vivo studies of QingDai (indigo naturalis) promotes mucosal healing and symptom improvement in ulcerative colitis by regulating the AHR-Th17/Treg pathway. Regulatory role of microRNAs in virus-mediated inflammation. Influence and distinctions of particulate matter exposure across varying etiotypes in chronic obstructive pulmonary disease (COPD) mouse model. Profile of immune response during nasal challenge with dermatophagoides pteronyssinus in subjects with allergic airway diseases. Transcriptional pathways of terminal differentiation in high- and low-density blood granulocytes in sepsis.
×
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