Cargando…
Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF-β1/Smad Pathway
Epithelial-mesenchymal transition (EMT) is a process associated with airway remodeling in chronic obstructive pulmonary disease (COPD), which leads to progressive pulmonary destruction. Panax ginseng is a traditional herbal medicine that has been shown to improve pulmonary function and exercise capa...
Autores principales: | , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2017
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5572594/ https://www.ncbi.nlm.nih.gov/pubmed/29104873 http://dx.doi.org/10.1155/2017/7171404 |
_version_ | 1783259548115533824 |
---|---|
author | Guan, Sibin Xu, Weiguo Han, Fengfeng Gu, Wen Song, Lin Ye, Wenjing Liu, Qian Guo, Xuejun |
author_facet | Guan, Sibin Xu, Weiguo Han, Fengfeng Gu, Wen Song, Lin Ye, Wenjing Liu, Qian Guo, Xuejun |
author_sort | Guan, Sibin |
collection | PubMed |
description | Epithelial-mesenchymal transition (EMT) is a process associated with airway remodeling in chronic obstructive pulmonary disease (COPD), which leads to progressive pulmonary destruction. Panax ginseng is a traditional herbal medicine that has been shown to improve pulmonary function and exercise capacity in patients with COPD. Ginsenoside Rg1 is one of the main active components and was shown to inhibit oxidative stress and inflammation. The present study investigated the hypothesis that ginsenoside Rg1 attenuates EMT in COPD rats induced by cigarette smoke (CS) and human bronchial epithelial (HBE) cells exposed to cigarette smoke extract (CSE). Our data showed that CS or CSE exposure increased expression of the mesenchymal marker α-smooth muscle actin (α-SMA) and decreased expression of the epithelial marker epithelial cadherin (E-cad) in both lung tissues and HBE cells, which was markedly suppressed by ginsenoside Rg1. Importantly, CS-induced upregulation of TGF-β1/Smad pathway components, including TGF-β1, TGF-βR1, phospho-Smad2, and phospho-Smad3, was also inhibited by ginsenoside Rg1. Additionally, ginsenoside Rg1 mimicked the effect of SB525334, a TGF-βR1-Smad2/3 inhibitor, on suppression of EMT in CSE-induced HBE cells. Collectively, we concluded that ginsenoside Rg1 alleviates CS-induced pulmonary EMT, in both COPD rats and HBE cells, via inhibition of the TGF-β1/Smad pathway. |
format | Online Article Text |
id | pubmed-5572594 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-55725942017-11-05 Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF-β1/Smad Pathway Guan, Sibin Xu, Weiguo Han, Fengfeng Gu, Wen Song, Lin Ye, Wenjing Liu, Qian Guo, Xuejun Biomed Res Int Research Article Epithelial-mesenchymal transition (EMT) is a process associated with airway remodeling in chronic obstructive pulmonary disease (COPD), which leads to progressive pulmonary destruction. Panax ginseng is a traditional herbal medicine that has been shown to improve pulmonary function and exercise capacity in patients with COPD. Ginsenoside Rg1 is one of the main active components and was shown to inhibit oxidative stress and inflammation. The present study investigated the hypothesis that ginsenoside Rg1 attenuates EMT in COPD rats induced by cigarette smoke (CS) and human bronchial epithelial (HBE) cells exposed to cigarette smoke extract (CSE). Our data showed that CS or CSE exposure increased expression of the mesenchymal marker α-smooth muscle actin (α-SMA) and decreased expression of the epithelial marker epithelial cadherin (E-cad) in both lung tissues and HBE cells, which was markedly suppressed by ginsenoside Rg1. Importantly, CS-induced upregulation of TGF-β1/Smad pathway components, including TGF-β1, TGF-βR1, phospho-Smad2, and phospho-Smad3, was also inhibited by ginsenoside Rg1. Additionally, ginsenoside Rg1 mimicked the effect of SB525334, a TGF-βR1-Smad2/3 inhibitor, on suppression of EMT in CSE-induced HBE cells. Collectively, we concluded that ginsenoside Rg1 alleviates CS-induced pulmonary EMT, in both COPD rats and HBE cells, via inhibition of the TGF-β1/Smad pathway. Hindawi 2017 2017-08-13 /pmc/articles/PMC5572594/ /pubmed/29104873 http://dx.doi.org/10.1155/2017/7171404 Text en Copyright © 2017 Sibin Guan et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Guan, Sibin Xu, Weiguo Han, Fengfeng Gu, Wen Song, Lin Ye, Wenjing Liu, Qian Guo, Xuejun Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF-β1/Smad Pathway |
title | Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF-β1/Smad Pathway |
title_full | Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF-β1/Smad Pathway |
title_fullStr | Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF-β1/Smad Pathway |
title_full_unstemmed | Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF-β1/Smad Pathway |
title_short | Ginsenoside Rg1 Attenuates Cigarette Smoke-Induced Pulmonary Epithelial-Mesenchymal Transition via Inhibition of the TGF-β1/Smad Pathway |
title_sort | ginsenoside rg1 attenuates cigarette smoke-induced pulmonary epithelial-mesenchymal transition via inhibition of the tgf-β1/smad pathway |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5572594/ https://www.ncbi.nlm.nih.gov/pubmed/29104873 http://dx.doi.org/10.1155/2017/7171404 |
work_keys_str_mv | AT guansibin ginsenosiderg1attenuatescigarettesmokeinducedpulmonaryepithelialmesenchymaltransitionviainhibitionofthetgfb1smadpathway AT xuweiguo ginsenosiderg1attenuatescigarettesmokeinducedpulmonaryepithelialmesenchymaltransitionviainhibitionofthetgfb1smadpathway AT hanfengfeng ginsenosiderg1attenuatescigarettesmokeinducedpulmonaryepithelialmesenchymaltransitionviainhibitionofthetgfb1smadpathway AT guwen ginsenosiderg1attenuatescigarettesmokeinducedpulmonaryepithelialmesenchymaltransitionviainhibitionofthetgfb1smadpathway AT songlin ginsenosiderg1attenuatescigarettesmokeinducedpulmonaryepithelialmesenchymaltransitionviainhibitionofthetgfb1smadpathway AT yewenjing ginsenosiderg1attenuatescigarettesmokeinducedpulmonaryepithelialmesenchymaltransitionviainhibitionofthetgfb1smadpathway AT liuqian ginsenosiderg1attenuatescigarettesmokeinducedpulmonaryepithelialmesenchymaltransitionviainhibitionofthetgfb1smadpathway AT guoxuejun ginsenosiderg1attenuatescigarettesmokeinducedpulmonaryepithelialmesenchymaltransitionviainhibitionofthetgfb1smadpathway |