Cinnamic acid ameliorates platelet activating factor-induced airway epithelial cell apoptosis and inflammation by inhibiting TGF-β1/Smad signaling pathway in an in vitro model of asthma.

IF 1.4 4区医学 Q2 Medicine

Revista De Investigacion Clinica-Clinical and Translational Investigation Pub Date : 2026-01-01 Epub Date: 2026-01-20 DOI:10.1016/j.ric.2025.100033

Huiling Zhang, Yan Zheng, Xueru Liu

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引用次数: 0

Abstract

Background: Asthma is a common chronic respiratory disease characterized by persistent airway inflammation. This study investigated the role of cinnamic acid (CA) in an in vitro model of asthma and its mechanisms.

Methods: Human small airway epithelial cells (HSAECs) were stimulated with platelet-activating factor (PAF), then exposed to CA (20, 50, or 100μM). Cell viability and apoptosis were assessed using CCK-8 assay and flow cytometry. Inflammatory cytokine levels were measured by ELISA. Barrier function was evaluated via lucifer yellow permeability assay. Western blotting and RT-qPCR were used to measure levels of TGF-β1 pathway-related factors. To investigate whether CA acts through TGF-β1 inhibition, PAF-treated cells were co-incubated with CA and TGF-β1.

Results: CA treatment significantly reduced PAF-induced apoptosis in HSAECs. It also attenuated the PAF-induced upregulation of TNF-α, IL-1β, and IL-6 levels as well as the downregulation of PGE2 levels. CA improved epithelial barrier function by reducing permeability. CA downregulated TGF-β1 and Smad4 levels and inhibited Smad2 and Smad3 phosphorylation. Exogenous activation of TGF-β1 abolished the protective effects of CA against apoptosis, inflammation, and barrier integrity.

Conclusion: Our findings demonstrate that CA inhibits apoptosis, inflammation, and barrier dysfunction in asthmatic airway cells by inhibiting the TGF-β1/Smad pathway.

查看原文本刊更多论文

在哮喘体外模型中，肉桂酸通过抑制TGF-β1/Smad信号通路改善血小板活化因子诱导的气道上皮细胞凋亡和炎症。

背景：哮喘是一种常见的以持续气道炎症为特征的慢性呼吸道疾病。本研究探讨了肉桂酸（CA）在哮喘体外模型中的作用及其机制。方法：用血小板活化因子（PAF）刺激人小气道上皮细胞（HSAECs），然后暴露于CA（20、50或100μM）。采用CCK-8法和流式细胞术检测细胞活力和凋亡情况。ELISA法检测炎症细胞因子水平。用路西法黄渗透性试验评价屏障功能。Western blotting和RT-qPCR检测TGF-β1通路相关因子水平。为了研究CA是否通过抑制TGF-β1起作用，我们将paf处理的细胞与CA和TGF-β1共孵育。结果：CA处理可显著减少paf诱导的hsaec细胞凋亡。它还能减弱paf诱导的TNF-α、IL-1β和IL-6水平的上调以及PGE2水平的下调。CA通过降低通透性改善上皮屏障功能。CA下调TGF-β1和Smad4水平，抑制Smad2和Smad3磷酸化。TGF-β1的外源激活可消除CA对细胞凋亡、炎症和屏障完整性的保护作用。结论：CA通过抑制TGF-β1/Smad通路抑制哮喘气道细胞凋亡、炎症和屏障功能障碍。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Revista De Investigacion Clinica-Clinical and Translational Investigation 医学-医学：内科

CiteScore

3.00

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： The Revista de Investigación Clínica – Clinical and Translational Investigation (RIC-C&TI), publishes original clinical and biomedical research of interest to physicians in internal medicine, surgery, and any of their specialties. The Revista de Investigación Clínica – Clinical and Translational Investigation is the official journal of the National Institutes of Health of Mexico, which comprises a group of Institutes and High Specialty Hospitals belonging to the Ministery of Health. The journal is published both on-line and in printed version, appears bimonthly and publishes peer-reviewed original research articles as well as brief and in-depth reviews. All articles published are open access and can be immediately and permanently free for everyone to read and download. The journal accepts clinical and molecular research articles, short reports and reviews. Types of manuscripts: – Brief Communications – Research Letters – Original Articles – Brief Reviews – In-depth Reviews – Perspectives – Letters to the Editor