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3-环丙甲氧基-4-（二氟甲氧基）苯甲酸对 TGF-β1 诱导的体外上皮间质转化和博来霉素诱导的体内肺纤维化的抑制作用。

Inhibitory Effects of 3-Cyclopropylmethoxy-4-(difluoromethoxy) Benzoic Acid on TGF-β1-Induced Epithelial-Mesenchymal Transformation of In Vitro and Bleomycin-Induced Pulmonary Fibrosis In Vivo.

机构信息

Key Laboratory of Marine Drugs, Ministry of Education, School of Medicine and Pharmacy, Ocean University of China, Qingdao 266003, China.

Laboratory for Marine Drugs and Bioproducts, Pilot National Laboratory for Marine Science and Technology (Qingdao), Qingdao 266237, China.

出版信息

Int J Mol Sci. 2023 Mar 24;24(7):6172. doi: 10.3390/ijms24076172.

DOI:10.3390/ijms24076172
PMID:37047142
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10094315/
Abstract

Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease characterized by lung inflammation and excessive deposition of extracellular matrix components. Transforming growth factor-β1 (TGF-β1) induced epithelial-mesenchymal transformation of type 2 lung epithelial cells leads to excessive extracellular matrix deposition, which plays an important role in fibrosis. Our objective was to evaluate the effects of 3-cyclopropylmethoxy-4-(difluoromethoxy) benzoic acid (DGM) on pulmonary fibrosis and aimed to determine whether EMT plays a key role in the pathogenesis of pulmonary fibrosis and whether EMT can be used as a therapeutic target for DGM therapy to reduce IPF. Firstly, stimulation of in vitro cultured A549 cells to construct EMTs with TGF-β1. DGM treatment inhibited the expression of proteins such as α-SMA, vimentin, and collagen Ⅰ and increased the expression of E-cadherin. Accordingly, Smad2/3 phosphorylation levels were significantly reduced by DGM treatment. Secondly, models of tracheal instillation of bleomycin and DGM were used to treat rats to demonstrate their therapeutic effects, such as improving lung function, reducing lung inflammation and fibrosis, reducing collagen deposition, and reducing the expression of E-cadherin. In conclusion, DGM attenuates TGF-β1-induced EMT in A549 cells and bleomycin-induced pulmonary fibrosis in rats.

摘要

特发性肺纤维化（IPF）是一种进行性肺部疾病，其特征是肺部炎症和细胞外基质成分的过度沉积。转化生长因子-β1（TGF-β1）诱导 2 型肺上皮细胞上皮-间充质转化导致细胞外基质的过度沉积，这在纤维化中起重要作用。我们的目的是评估 3-环丙基甲氧基-4-（二氟甲氧基）苯甲酸（DGM）对肺纤维化的影响，并旨在确定 EMT 是否在肺纤维化发病机制中起关键作用，以及 EMT 是否可作为 DGM 治疗减少 IPF 的治疗靶点。首先，用 TGF-β1 刺激体外培养的 A549 细胞构建 EMTs。DGM 处理抑制了 α-SMA、波形蛋白和胶原 Ⅰ等蛋白的表达，并增加了 E-钙粘蛋白的表达。相应地，DGM 处理显著降低了 Smad2/3 的磷酸化水平。其次，使用博来霉素气管内滴注和 DGM 模型治疗大鼠，以证明其治疗效果，如改善肺功能、减轻肺炎症和纤维化、减少胶原沉积以及降低 E-钙粘蛋白的表达。总之，DGM 可减轻 TGF-β1 诱导的 A549 细胞 EMT 和博来霉素诱导的大鼠肺纤维化。

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