Xianglong Kong, Hui Li, Qi Hu, Yusheng Yan, Wenfang Tang, Yuling Tang and Zheyu Hu
Background: Idiopathic pulmonary fibrosis (IPF) is an incurable, progressive, and fatal interstitial lung disease with the characteristics of lung tissue damage and an enhancement in extracellular matrix (ECM). Alveolar epithelial cells (AMs) are major target cells that can directly promote to occurring of pulmonary fibrosis by acquisition of a mesenchymal phenotype through epithelial- mesenchymal transition (EMT). Neferine, a component of Chinese herbs, has been thought to be involved in anti-fibrotic activity in experimental lung fibrosis. However, its mechanism is not clear. In this study, we explore the regulation of neferine in TGF-β-induced EMT in lung fibrosis model and illustrate its mechanism of action.
Methods: The alveolar epithelial cell line A549 was stimulated with TGF-β1 with or without Neferine pretreatment in advance. Morphologic variations and expression of EMT-related markers, including E-cadherin, β-catenina-SMA and Vimentin were detected. Expressions of Smad2, p- Smad 2, Smad3 and p-Smad3 were measured.
Results: TGF-β1–treated A549 cells were transformed into the mesenchymal morphology with less E-cadherin, β-catenin and more a-SMA, Vimentin expression. The addition of Neferine inhibited the TGF-β1–induced change of the mesenchymal phenotype. Furthermore, Neferine inhibited the TGF-β1–induced increase in the expression of p- Smad2 and p-Smad3.
Conclusions: Our study illustrate that Neferine inhibits TGF-β1–induced EMT in lung fibrosis model via TGF-β signaling pathway.