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Corilagin Attenuates Aerosol Bleomycin-Induced Experimental Lung Injury
Idiopathic pulmonary fibrosis (IPF) is a progressing lethal disease with few clinically effective therapies. Corilagin is a tannin derivative which shows anti-inflammatory and antifibrotics properties and is potentiated in treating IPF. Here, we investigated the effect of corilagin on lung injury fo...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4100119/ https://www.ncbi.nlm.nih.gov/pubmed/24886817 http://dx.doi.org/10.3390/ijms15069762 |
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author | Wang, Zheng Guo, Qiong-Ya Zhang, Xiao-Ju Li, Xiao Li, Wen-Ting Ma, Xi-Tao Ma, Li-Jun |
author_facet | Wang, Zheng Guo, Qiong-Ya Zhang, Xiao-Ju Li, Xiao Li, Wen-Ting Ma, Xi-Tao Ma, Li-Jun |
author_sort | Wang, Zheng |
collection | PubMed |
description | Idiopathic pulmonary fibrosis (IPF) is a progressing lethal disease with few clinically effective therapies. Corilagin is a tannin derivative which shows anti-inflammatory and antifibrotics properties and is potentiated in treating IPF. Here, we investigated the effect of corilagin on lung injury following bleomycin exposure in an animal model of pulmonary fibrosis. Corilagin abrogated bleomycin-induced lung fibrosis as assessed by H&E; Masson’s trichrome staining and lung hydroxyproline content in lung tissue. Corilagin reduced the number of apoptotic lung cells and prevented lung epithelial cells from membrane breakdown, effluence of lamellar bodies and thickening of the respiratory membrane. Bleomycin exposure induced expression of MDA, IKKα, phosphorylated IKKα (p-IKKα), NF-κB P65, TNF-α and IL-1β, and reduced I-κB expression in mice lung tissue or in BALF. These changes were reversed by high-dose corilagin (100 mg/kg i.p) more dramatically than by low dose (10 mg/kg i.p). Last, corilagin inhibits TGF-β1 production and α-SMA expression in lung tissue samples. Taken together, these findings confirmed that corilagin attenuates bleomycin-induced epithelial injury and fibrosis via inactivation of oxidative stress, proinflammatory cytokine release and NF-κB and TGF-β1 signaling. Corilagin may serve as a promising therapeutic agent for pulmonary fibrosis. |
format | Online Article Text |
id | pubmed-4100119 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-41001192014-07-16 Corilagin Attenuates Aerosol Bleomycin-Induced Experimental Lung Injury Wang, Zheng Guo, Qiong-Ya Zhang, Xiao-Ju Li, Xiao Li, Wen-Ting Ma, Xi-Tao Ma, Li-Jun Int J Mol Sci Article Idiopathic pulmonary fibrosis (IPF) is a progressing lethal disease with few clinically effective therapies. Corilagin is a tannin derivative which shows anti-inflammatory and antifibrotics properties and is potentiated in treating IPF. Here, we investigated the effect of corilagin on lung injury following bleomycin exposure in an animal model of pulmonary fibrosis. Corilagin abrogated bleomycin-induced lung fibrosis as assessed by H&E; Masson’s trichrome staining and lung hydroxyproline content in lung tissue. Corilagin reduced the number of apoptotic lung cells and prevented lung epithelial cells from membrane breakdown, effluence of lamellar bodies and thickening of the respiratory membrane. Bleomycin exposure induced expression of MDA, IKKα, phosphorylated IKKα (p-IKKα), NF-κB P65, TNF-α and IL-1β, and reduced I-κB expression in mice lung tissue or in BALF. These changes were reversed by high-dose corilagin (100 mg/kg i.p) more dramatically than by low dose (10 mg/kg i.p). Last, corilagin inhibits TGF-β1 production and α-SMA expression in lung tissue samples. Taken together, these findings confirmed that corilagin attenuates bleomycin-induced epithelial injury and fibrosis via inactivation of oxidative stress, proinflammatory cytokine release and NF-κB and TGF-β1 signaling. Corilagin may serve as a promising therapeutic agent for pulmonary fibrosis. MDPI 2014-05-30 /pmc/articles/PMC4100119/ /pubmed/24886817 http://dx.doi.org/10.3390/ijms15069762 Text en © 2014 by the authors; licensee MDPI, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0/ This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). |
spellingShingle | Article Wang, Zheng Guo, Qiong-Ya Zhang, Xiao-Ju Li, Xiao Li, Wen-Ting Ma, Xi-Tao Ma, Li-Jun Corilagin Attenuates Aerosol Bleomycin-Induced Experimental Lung Injury |
title | Corilagin Attenuates Aerosol Bleomycin-Induced Experimental Lung Injury |
title_full | Corilagin Attenuates Aerosol Bleomycin-Induced Experimental Lung Injury |
title_fullStr | Corilagin Attenuates Aerosol Bleomycin-Induced Experimental Lung Injury |
title_full_unstemmed | Corilagin Attenuates Aerosol Bleomycin-Induced Experimental Lung Injury |
title_short | Corilagin Attenuates Aerosol Bleomycin-Induced Experimental Lung Injury |
title_sort | corilagin attenuates aerosol bleomycin-induced experimental lung injury |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4100119/ https://www.ncbi.nlm.nih.gov/pubmed/24886817 http://dx.doi.org/10.3390/ijms15069762 |
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