Rhizoma coptidis can inhibit the excessive proliferation, inflammation, and transformation of lung fibroblasts into myofibroblasts.

IF 2.5 4区 医学 Q3 ALLERGY
Allergologia et immunopathologia Pub Date : 2024-07-01 eCollection Date: 2024-01-01 DOI:10.15586/aei.v52i4.1111
Jie Yang, Yuting Huang, Zhimin Cui, Chang Liu, Guofang Xie
{"title":"Rhizoma coptidis can inhibit the excessive proliferation, inflammation, and transformation of lung fibroblasts into myofibroblasts.","authors":"Jie Yang, Yuting Huang, Zhimin Cui, Chang Liu, Guofang Xie","doi":"10.15586/aei.v52i4.1111","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Pulmonary fibrosis (PF) is a chronic, progressive, and irreversible heterogeneous disease of lung interstitial tissue. To combat progression of PF, new drugs are required to be developed. Rhizoma coptidis (COP), one of the main alkaloids of Coptis chinensis, is a traditional herbal medicine used to treat various inflammatory diseases.</p><p><strong>Objective: </strong>To investigate the possible effects of Coptisine (Cop) on the growth, inflammation, as well as FMT of TNF-β1-induced HFL1 cells and uncover the mechanism.</p><p><strong>Material and methods: </strong>Human fetal lung fibroblast 1 (HFL1) was induced using 6ng/mL TGF-β1 as a model of pulmonary fibrosis. CCK-8, Brdu, and transwell assays indicated the effects on cell growth as well as motility. qPCR and the corresponding kits indicted the effects on cell inflammation. Immunoblot showed the effects on FMT and further confirmed the mechanism.</p><p><strong>Results: </strong>Coptisine inhibits excessive growth as well as motility of TNF-β1-induced HFL1 cells. It further inhibits inflammation and ROS levels in TNF-β1-induced HFL1 cells. Coptisine inhibits the FMT process of TNF-β1-induced HFL1 cells. Mechanically, coptisine promotes the Nrf2/HO-1 pathway.</p><p><strong>Conclusion: </strong>Coptisine can inhibit the excessive growth, inflammation as well as FMT of lung fibroblasts into myofibroblasts. It could serve as a promising drug of PF.</p>","PeriodicalId":7536,"journal":{"name":"Allergologia et immunopathologia","volume":null,"pages":null},"PeriodicalIF":2.5000,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Allergologia et immunopathologia","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.15586/aei.v52i4.1111","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"ALLERGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Pulmonary fibrosis (PF) is a chronic, progressive, and irreversible heterogeneous disease of lung interstitial tissue. To combat progression of PF, new drugs are required to be developed. Rhizoma coptidis (COP), one of the main alkaloids of Coptis chinensis, is a traditional herbal medicine used to treat various inflammatory diseases.

Objective: To investigate the possible effects of Coptisine (Cop) on the growth, inflammation, as well as FMT of TNF-β1-induced HFL1 cells and uncover the mechanism.

Material and methods: Human fetal lung fibroblast 1 (HFL1) was induced using 6ng/mL TGF-β1 as a model of pulmonary fibrosis. CCK-8, Brdu, and transwell assays indicated the effects on cell growth as well as motility. qPCR and the corresponding kits indicted the effects on cell inflammation. Immunoblot showed the effects on FMT and further confirmed the mechanism.

Results: Coptisine inhibits excessive growth as well as motility of TNF-β1-induced HFL1 cells. It further inhibits inflammation and ROS levels in TNF-β1-induced HFL1 cells. Coptisine inhibits the FMT process of TNF-β1-induced HFL1 cells. Mechanically, coptisine promotes the Nrf2/HO-1 pathway.

Conclusion: Coptisine can inhibit the excessive growth, inflammation as well as FMT of lung fibroblasts into myofibroblasts. It could serve as a promising drug of PF.

黄连能抑制肺成纤维细胞的过度增殖、炎症和向肌成纤维细胞的转化。
背景:肺纤维化(PF)是一种慢性、进行性和不可逆的肺间质组织异质性疾病。为遏制肺纤维化的进展,需要开发新的药物。黄连(COP)是黄连的主要生物碱之一,是一种用于治疗各种炎症性疾病的传统草药:材料与方法:以 6ng/mL TGF-β1 为肺纤维化模型,诱导人胎肺成纤维细胞 1(HFL1)。CCK-8、Brdu 和 transwell 试验表明了对细胞生长和运动的影响。免疫印迹显示了对 FMT 的影响,并进一步证实了其机制:结果:黄连素可抑制 TNF-β1 诱导的 HFL1 细胞的过度生长和运动。结果:黄连素可抑制 TNF-β1 诱导的 HFL1 细胞的过度生长和运动,进一步抑制 TNF-β1 诱导的 HFL1 细胞的炎症和 ROS 水平。黄连素可抑制 TNF-β1 诱导的 HFL1 细胞的 FMT 过程。结论:黄连素能抑制TNF-β1诱导的HFL1细胞的FMT过程:结论:黄连素可抑制肺成纤维细胞的过度生长、炎症以及向肌成纤维细胞的FMT转化。结论:黄连素可抑制肺成纤维细胞的过度生长和炎症反应,并可抑制肺成纤维细胞向肌成纤维细胞的转化。
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
CiteScore
3.70
自引率
0.00%
发文量
131
审稿时长
6-12 weeks
期刊介绍: Founded in 1972 by Professor A. Oehling, Allergologia et Immunopathologia is a forum for those working in the field of pediatric asthma, allergy and immunology. Manuscripts related to clinical, epidemiological and experimental allergy and immunopathology related to childhood will be considered for publication. Allergologia et Immunopathologia is the official journal of the Spanish Society of Pediatric Allergy and Clinical Immunology (SEICAP) and also of the Latin American Society of Immunodeficiencies (LASID). It has and independent international Editorial Committee which submits received papers for peer-reviewing by international experts. The journal accepts original and review articles from all over the world, together with consensus statements from the aforementioned societies. Occasionally, the opinion of an expert on a burning topic is published in the "Point of View" section. Letters to the Editor on previously published papers are welcomed. Allergologia et Immunopathologia publishes 6 issues per year and is included in the major databases such as Pubmed, Scopus, Web of Knowledge, etc.
×
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