Treatment effects of the traditional Chinese medicine Shenks in bleomycin-induced lung fibrosis through regulation of TGF-beta/Smad3 signaling and oxidative stress

Abstract Pulmonary fibrosis is a kind of devastating interstitial lung disease due to the limited therapeutic strategies. Traditional Chinese medicine (TCM) practices have put forth Shenks as a promising treatment approach. Here, we performed in vivo study and in vitro study to delineate the anti-fi...

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Autores principales: Haiyan Chu, Ying Shi, Shuai Jiang, Qicheng Zhong, Yongqiang Zhao, Qingmei Liu, Yanyun Ma, Xiangguang Shi, Weifeng Ding, Xiaodong Zhou, Jimin Cui, Li Jin, Gang Guo, Jiucun Wang
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Publicado: Nature Portfolio 2017
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spelling oai:doaj.org-article:0facbc85898245e5ac42ab18e616186d2021-12-02T11:51:11ZTreatment effects of the traditional Chinese medicine Shenks in bleomycin-induced lung fibrosis through regulation of TGF-beta/Smad3 signaling and oxidative stress10.1038/s41598-017-02293-z2045-2322https://doaj.org/article/0facbc85898245e5ac42ab18e616186d2017-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-02293-zhttps://doaj.org/toc/2045-2322Abstract Pulmonary fibrosis is a kind of devastating interstitial lung disease due to the limited therapeutic strategies. Traditional Chinese medicine (TCM) practices have put forth Shenks as a promising treatment approach. Here, we performed in vivo study and in vitro study to delineate the anti-fibrotic mechanisms behind Shenks treatment for pulmonary fibrosis. We found that regardless of the prophylactic or therapeutic treatment, Shenks was able to attenuate BLM-induced-fibrosis in mice, down regulate extracellular matrix genes expression, and reduce collagen production. The aberrantly high Smad3 phosphorylation levels and SBE activity in TGF-β-induced fibroblasts were dramatically decreased as a result of Shenks treatment. At the same time, Shenks was able to increase the expression of antioxidant-related genes, including Gclc and Ec-sod, while reduce the transcription levels of oxidative-related genes, such as Rac1 and Nox4 demonstrated by both in vivo and in vitro studies. Further investigations found that Shenks could decrease the oxidative productions of protein (3-nitrotyrosine) and lipid (malondialdehyde) and increase GSH content both in bleomycin treated mouse lungs and TGF-β stimulated fibroblasts, as well as inhibit the production of ROS stimulated by TGF-β to fight against oxidative stress. Overall, Shenks inhibited fibrosis by blocking TGF-β pathway and modulating the oxidant/antioxidant balance.Haiyan ChuYing ShiShuai JiangQicheng ZhongYongqiang ZhaoQingmei LiuYanyun MaXiangguang ShiWeifeng DingXiaodong ZhouJimin CuiLi JinGang GuoJiucun WangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Haiyan Chu
Ying Shi
Shuai Jiang
Qicheng Zhong
Yongqiang Zhao
Qingmei Liu
Yanyun Ma
Xiangguang Shi
Weifeng Ding
Xiaodong Zhou
Jimin Cui
Li Jin
Gang Guo
Jiucun Wang
Treatment effects of the traditional Chinese medicine Shenks in bleomycin-induced lung fibrosis through regulation of TGF-beta/Smad3 signaling and oxidative stress
description Abstract Pulmonary fibrosis is a kind of devastating interstitial lung disease due to the limited therapeutic strategies. Traditional Chinese medicine (TCM) practices have put forth Shenks as a promising treatment approach. Here, we performed in vivo study and in vitro study to delineate the anti-fibrotic mechanisms behind Shenks treatment for pulmonary fibrosis. We found that regardless of the prophylactic or therapeutic treatment, Shenks was able to attenuate BLM-induced-fibrosis in mice, down regulate extracellular matrix genes expression, and reduce collagen production. The aberrantly high Smad3 phosphorylation levels and SBE activity in TGF-β-induced fibroblasts were dramatically decreased as a result of Shenks treatment. At the same time, Shenks was able to increase the expression of antioxidant-related genes, including Gclc and Ec-sod, while reduce the transcription levels of oxidative-related genes, such as Rac1 and Nox4 demonstrated by both in vivo and in vitro studies. Further investigations found that Shenks could decrease the oxidative productions of protein (3-nitrotyrosine) and lipid (malondialdehyde) and increase GSH content both in bleomycin treated mouse lungs and TGF-β stimulated fibroblasts, as well as inhibit the production of ROS stimulated by TGF-β to fight against oxidative stress. Overall, Shenks inhibited fibrosis by blocking TGF-β pathway and modulating the oxidant/antioxidant balance.
format article
author Haiyan Chu
Ying Shi
Shuai Jiang
Qicheng Zhong
Yongqiang Zhao
Qingmei Liu
Yanyun Ma
Xiangguang Shi
Weifeng Ding
Xiaodong Zhou
Jimin Cui
Li Jin
Gang Guo
Jiucun Wang
author_facet Haiyan Chu
Ying Shi
Shuai Jiang
Qicheng Zhong
Yongqiang Zhao
Qingmei Liu
Yanyun Ma
Xiangguang Shi
Weifeng Ding
Xiaodong Zhou
Jimin Cui
Li Jin
Gang Guo
Jiucun Wang
author_sort Haiyan Chu
title Treatment effects of the traditional Chinese medicine Shenks in bleomycin-induced lung fibrosis through regulation of TGF-beta/Smad3 signaling and oxidative stress
title_short Treatment effects of the traditional Chinese medicine Shenks in bleomycin-induced lung fibrosis through regulation of TGF-beta/Smad3 signaling and oxidative stress
title_full Treatment effects of the traditional Chinese medicine Shenks in bleomycin-induced lung fibrosis through regulation of TGF-beta/Smad3 signaling and oxidative stress
title_fullStr Treatment effects of the traditional Chinese medicine Shenks in bleomycin-induced lung fibrosis through regulation of TGF-beta/Smad3 signaling and oxidative stress
title_full_unstemmed Treatment effects of the traditional Chinese medicine Shenks in bleomycin-induced lung fibrosis through regulation of TGF-beta/Smad3 signaling and oxidative stress
title_sort treatment effects of the traditional chinese medicine shenks in bleomycin-induced lung fibrosis through regulation of tgf-beta/smad3 signaling and oxidative stress
publisher Nature Portfolio
publishDate 2017
url https://doaj.org/article/0facbc85898245e5ac42ab18e616186d
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