Serum containing drugs of Gua Lou Xie Bai decoction (GLXB-D) can inhibit TGF-β1-Induced Epithelial to Mesenchymal Transition (EMT) in A549 Cells
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 alveol...
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De Gruyter
2018-05-01
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Series: | Open Chemistry |
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Online Access: | https://doi.org/10.1515/chem-2018-0042 |
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author | Li Rui-qin Wang Bai-yan Ding Yu-wen Zhang Rui Zhang Jun-xia Lu Xiao-kang |
author_facet | Li Rui-qin Wang Bai-yan Ding Yu-wen Zhang Rui Zhang Jun-xia Lu Xiao-kang |
author_sort | Li Rui-qin |
collection | DOAJ |
description | 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. |
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spelling | doaj.art-0f26392d8185428c87739b1a6c07deb82022-12-21T21:30:25ZengDe GruyterOpen Chemistry2391-54202018-05-0116140741410.1515/chem-2018-0042chem-2018-0042Serum containing drugs of Gua Lou Xie Bai decoction (GLXB-D) can inhibit TGF-β1-Induced Epithelial to Mesenchymal Transition (EMT) in A549 CellsLi Rui-qin0Wang Bai-yan1Ding Yu-wen2Zhang Rui3Zhang Jun-xia4Lu Xiao-kang5Scientific Research Pathological Experiment Center, Henan University of Chinese Medicine, Zhengzhou, China, 450046Key Discipline Laboratory of Basic Medicine, Henan University of Chinese Medicine, Zhengzhou, China, 450046Scientific Research Pathological Experiment Center, Henan University of Chinese Medicine, Zhengzhou, China, 450046Scientific Research Pathological Experiment Center, Henan University of Chinese Medicine, Zhengzhou, China, 450046Scientific Research Pathological Experiment Center, Henan University of Chinese Medicine, Zhengzhou, China, 450046Scientific Research Pathological Experiment Center, Henan University of Chinese Medicine, Zhengzhou, China, 450046The 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.https://doi.org/10.1515/chem-2018-0042pulmonary fibrosistgf-β1emtglxb-d |
spellingShingle | Li Rui-qin Wang Bai-yan Ding Yu-wen Zhang Rui Zhang Jun-xia Lu Xiao-kang Serum containing drugs of Gua Lou Xie Bai decoction (GLXB-D) can inhibit TGF-β1-Induced Epithelial to Mesenchymal Transition (EMT) in A549 Cells Open Chemistry pulmonary fibrosis tgf-β1 emt glxb-d |
title | Serum containing drugs of Gua Lou Xie Bai decoction (GLXB-D) can inhibit TGF-β1-Induced Epithelial to Mesenchymal Transition (EMT) in A549 Cells |
title_full | Serum containing drugs of Gua Lou Xie Bai decoction (GLXB-D) can inhibit TGF-β1-Induced Epithelial to Mesenchymal Transition (EMT) in A549 Cells |
title_fullStr | Serum containing drugs of Gua Lou Xie Bai decoction (GLXB-D) can inhibit TGF-β1-Induced Epithelial to Mesenchymal Transition (EMT) in A549 Cells |
title_full_unstemmed | Serum containing drugs of Gua Lou Xie Bai decoction (GLXB-D) can inhibit TGF-β1-Induced Epithelial to Mesenchymal Transition (EMT) in A549 Cells |
title_short | Serum containing drugs of Gua Lou Xie Bai decoction (GLXB-D) can inhibit TGF-β1-Induced Epithelial to Mesenchymal Transition (EMT) in A549 Cells |
title_sort | serum containing drugs of gua lou xie bai decoction glxb d can inhibit tgf β1 induced epithelial to mesenchymal transition emt in a549 cells |
topic | pulmonary fibrosis tgf-β1 emt glxb-d |
url | https://doi.org/10.1515/chem-2018-0042 |
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