Serum containing drugs of Gua Lou Xie Bai decoction (GLXB-D) can inhibit TGF-β1-Induced Epithelial to Mesenchymal Transition (EMT) in A549 Cells
Autor: | Bai-yan Wang, Yu-wen Ding, Xiao-kang Lu, Jun-xia Zhang, Rui-qin Li, Rui Zhang |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
A549 cell pulmonary fibrosis Chemistry tgf-β1 emt Decoction General Chemistry glxb-d medicine.disease 03 medical and health sciences 030104 developmental biology Pulmonary fibrosis Materials Chemistry Cancer research medicine Epithelial–mesenchymal transition QD1-999 Transforming growth factor |
Zdroj: | Open Chemistry, Vol 16, Iss 1, Pp 407-414 (2018) |
ISSN: | 2391-5420 |
Popis: | The present study explores the mechanism of resistance to pulmonary fibrosis by observing the possible effects of serum containing drugs prepared from Gua Lou Xie Bai decoction (GLXB-D) on transforming growth factor beta 1 (TGF-β1) induced Epithelial-mesenchymal transition (EMT) of A549 human alveolar epithelial cells. The inhibition rate was observed with the help of thiazolyl blue tetrazolium bromide (MTT) in 24 h and 48 h treated cells. Inverted microscope and transmission electron microscope (TEM) were used to study the changes in the morphology and ultrastructure of the cells. The expressions of E-cadherin and Vimentin were comparatively analyzed by Western blotting, while the expressions of Collagen I and III were analyzed by ELISA. The data obtained indicated that the expression of epithelial marker E-cadherin was decreased, while the expressions of EMT markers such as Vimentin and Collagen I and III were increased in 24 h after TGF-β1 induction. However, the serum containing drugs of GLXB-D were found to inhibit the TGF-β1 induced proliferation of cells, increase the expression of E-cadherin and decrease the expression of Vimentin, collagen I and III. In conclusion, the serum containing drugs of GLXB-D effectively reduced pulmonary fibrosis, mainly via the reversal of EMT induction by TGF-β1. Thus, it can be considered as a potential candidate for the development of better treatment methods for pulmonary fibrosis. |
Databáze: | OpenAIRE |
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