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 Journal of the Renin-Angiotensin-Aldosterone System Pub Date : 2021-01-01 DOI:10.1177/14703203211003786
Xiwen Zang, Jun Zhao, Chengzhi Lu
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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.

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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。
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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.
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