PM2.5 inducing myocardial fibrosis mediated by Ang II/ERK1/2/TGF-β1 signaling pathway in mice model.

IF 2.1 4区 医学 Q3 PERIPHERAL VASCULAR DISEASE
Xiwen Zang, Jun Zhao, Chengzhi Lu
{"title":"PM2.5 inducing myocardial fibrosis mediated by Ang II/ERK1/2/TGF-β<sub>1</sub> signaling pathway in mice model.","authors":"Xiwen Zang, Jun Zhao, Chengzhi Lu","doi":"10.1177/14703203211003786","DOIUrl":null,"url":null,"abstract":"<p><strong>Objects: </strong>To discuss the influence of PM2.5 on myocardial fibrosis and related mechanism.</p><p><strong>Methods: </strong>PM2.5 particles were prepared into different concentrations of solution to drip into the mice's trachea twice each week. The mice were divided into five groups, Blank control group (C group), NS control group (J group), high dose group (G group, 10 mg/kg), medium dose group (Z group, 5 mg/kg), and 1ow dose group (D group, 2.5 mg/kg). After 6 weeks, the myocardial fibrosis was observed by HE and Masson staining. The expression of Ang II, ERK1/2, and TGF-β<sub>1</sub> was examined by Western Blotting (WB) and Real time PCR (RT-PCR).</p><p><strong>Results: </strong>The higher dose PM2.5 was administrated, the worse the myocardial fibrosis was in PM2.5 groups. The expression of Ang II, ERK1/2, and TGF-β<sub>1</sub> was increased in higher dose groups in protein and mRNA level.</p><p><strong>Conclusion: </strong>1. PM2.5 induced the cardiac fibrosis. 2. PM2.5 dripped into trachea in mice model activated the expression of Ang II, ERK1/2, and TGF-β<sub>1</sub>. The activation of renin-angiotensin system (RAS) was suggested to participate in the cardiac fibrosis induced by PM2.5.</p>","PeriodicalId":17330,"journal":{"name":"Journal of the Renin-Angiotensin-Aldosterone System","volume":"22 1","pages":"14703203211003786"},"PeriodicalIF":2.1000,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0d/f3/10.1177_14703203211003786.PMC7983242.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of the Renin-Angiotensin-Aldosterone System","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1177/14703203211003786","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PERIPHERAL VASCULAR DISEASE","Score":null,"Total":0}
引用次数: 0

Abstract

Objects: To discuss the influence of PM2.5 on myocardial fibrosis and related mechanism.

Methods: PM2.5 particles were prepared into different concentrations of solution to drip into the mice's trachea twice each week. The mice were divided into five groups, Blank control group (C group), NS control group (J group), high dose group (G group, 10 mg/kg), medium dose group (Z group, 5 mg/kg), and 1ow dose group (D group, 2.5 mg/kg). After 6 weeks, the myocardial fibrosis was observed by HE and Masson staining. The expression of Ang II, ERK1/2, and TGF-β1 was examined by Western Blotting (WB) and Real time PCR (RT-PCR).

Results: The higher dose PM2.5 was administrated, the worse the myocardial fibrosis was in PM2.5 groups. The expression of Ang II, ERK1/2, and TGF-β1 was increased in higher dose groups in protein and mRNA level.

Conclusion: 1. PM2.5 induced the cardiac fibrosis. 2. PM2.5 dripped into trachea in mice model activated the expression of Ang II, ERK1/2, and TGF-β1. The activation of renin-angiotensin system (RAS) was suggested to participate in the cardiac fibrosis induced by PM2.5.

Abstract Image

Abstract Image

Abstract Image

在小鼠模型中,PM2.5 通过 Ang II/ERK1/2/TGF-β1 信号通路诱导心肌纤维化。
目的:探讨PM2.5对心肌纤维化的影响及相关机制:探讨PM2.5对心肌纤维化的影响及相关机制:将PM2.5颗粒配制成不同浓度的溶液滴入小鼠气管,每周两次。小鼠分为五组,分别为空白对照组(C组)、NS对照组(J组)、高剂量组(G组,10 mg/kg)、中剂量组(Z组,5 mg/kg)和低剂量组(D组,2.5 mg/kg)。6周后,用HE和Masson染色法观察心肌纤维化。Western Blotting (WB)和Real time PCR (RT-PCR)检测了Ang II、ERK1/2和TGF-β1的表达:结果:PM2.5剂量越高,PM2.5组心肌纤维化越严重。结论:1.PM2.5诱导心肌纤维化。2.2. PM2.5滴入小鼠气管模型激活了Ang II、ERK1/2和TGF-β1的表达。肾素-血管紧张素系统(RAS)的激活被认为参与了PM2.5诱导的心脏纤维化。
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
6.20
自引率
0.00%
发文量
16
审稿时长
6-12 weeks
期刊介绍: JRAAS is a peer-reviewed, open access journal, serving as a resource for biomedical professionals, primarily with an active interest in the renin-angiotensin-aldosterone system in humans and other mammals. It publishes original research and reviews on the normal and abnormal function of this system and its pharmacology and therapeutics, mostly in a cardiovascular context but including research in all areas where this system is present, including the brain, lungs and gastro-intestinal tract.
×
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