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Mechanism of the effect of tanshinone IIA epithelial-mesenchymal transition via the TGF-β1/smad pathway in human alveolar epithelial cell line A549

Bai-Yan Wang, Yan Jin, Cai-Li Zhang, Jun-Xia Zhang, Li-Min Sun, Ying-Ke Guo, Rui-Qin Li

This study aimed to investigate the inhibitory effects of the different concentrations of Tanshinone IIA (Tan IIA) on the proliferation of human alveolar epithelial cell line A549 and its regulatory mechanism in epithelial-mesenchymal transition (EMT). The proliferation activity of cells was examined using the thiazolyl blue tetrazolium bromide (MTT) method. The changes in the expression of epithelial cell marker protein E-cadherin (E-cad) and interstitial marker protein alpha-smooth muscle actin (α-SMA) were detected using the cellular immunochemical method. The changes in cell morphology and ultrastructure were observed under the inverted microscope and transmission electron microscope, respectively. Western blot analysis was used to detect the expression of E-cad, α-SMA, Smad7, and Smad3. The MTT assay showed that the cell viability in the transforming growth factor beta 1 (TGF-β1) induced group was higher than that in the normal group, but the difference was not obvious. However, the cell viability of the Tan IIA-treated groups obviously decreased compared with the TGF-β1-induced and normal groups. Meanwhile, the expression of E-cad and Smad7 decreased, and the expression of α- SMA and Smad3 increased after A549 cells were induced by 5 ng/mL TGF-β1 for 24 h. However, their expression levels were close to the expression level of the control group after the cells were treated with Tan IIA for 24 h. In conclusion, the results demonstrated that Tan IIA could inhibit EMT of alveolar epithelial cells induced by TGF-β1, probably by regulating the expression of TGF-β/Smad pathway protein. Therefore, Tan IIA might serve as a potential anti-fibrosis drug in treating pulmonary fibrosis.