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Isoflavone Aglycones Attenuate Cigarette Smoke-Induced Emphysema via Suppression of Neutrophilic Inflammation in a COPD Murine Model
Chronic obstructive pulmonary disease (COPD), a lung disease caused by chronic exposure to cigarette smoke, increases the number of inflammatory cells such as macrophages and neutrophils and emphysema. Isoflavone is a polyphenolic compound that exists in soybeans. Daidzein and genistein, two types o...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6769447/ https://www.ncbi.nlm.nih.gov/pubmed/31470503 http://dx.doi.org/10.3390/nu11092023 |
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author | Kojima, Kazuya Asai, Kazuhisa Kubo, Hiroaki Sugitani, Arata Kyomoto, Yohkoh Okamoto, Atsuko Yamada, Kazuhiro Ijiri, Naoki Watanabe, Tetsuya Hirata, Kazuto Kawaguchi, Tomoya |
author_facet | Kojima, Kazuya Asai, Kazuhisa Kubo, Hiroaki Sugitani, Arata Kyomoto, Yohkoh Okamoto, Atsuko Yamada, Kazuhiro Ijiri, Naoki Watanabe, Tetsuya Hirata, Kazuto Kawaguchi, Tomoya |
author_sort | Kojima, Kazuya |
collection | PubMed |
description | Chronic obstructive pulmonary disease (COPD), a lung disease caused by chronic exposure to cigarette smoke, increases the number of inflammatory cells such as macrophages and neutrophils and emphysema. Isoflavone is a polyphenolic compound that exists in soybeans. Daidzein and genistein, two types of isoflavones, have been reported to have anti-inflammatory effects in various organs. We hypothesized that the daidzein-rich soy isoflavone aglycones (DRIAs) attenuate cigarette smoke-induced emphysema in mice. Mice were divided into four groups: the (i) control group, (ii) isoflavone group, (iii) smoking group, and (iv) isoflavone + smoking group. The number of inflammatory cells in the bronchoalveolar lavage fluid (BALF) and the airspace enlargement using the mean linear intercept (MLI) were determined 12 weeks after smoking exposure. Expressions of neutrophilic inflammatory cytokines and chemokines were also examined. In the isoflavone + smoking group, the number of neutrophils in BALF and MLI was significantly less than that in the smoking group. Furthermore, the gene-expressions of TNF-α and CXCL2 (MIP-2) in the isoflavone + smoking group were significantly less than those in the smoking group. Supplementation of the COPD murine model with DRIAs significantly attenuates pathological changes of COPD via suppression of neutrophilic inflammation. |
format | Online Article Text |
id | pubmed-6769447 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-67694472019-10-30 Isoflavone Aglycones Attenuate Cigarette Smoke-Induced Emphysema via Suppression of Neutrophilic Inflammation in a COPD Murine Model Kojima, Kazuya Asai, Kazuhisa Kubo, Hiroaki Sugitani, Arata Kyomoto, Yohkoh Okamoto, Atsuko Yamada, Kazuhiro Ijiri, Naoki Watanabe, Tetsuya Hirata, Kazuto Kawaguchi, Tomoya Nutrients Article Chronic obstructive pulmonary disease (COPD), a lung disease caused by chronic exposure to cigarette smoke, increases the number of inflammatory cells such as macrophages and neutrophils and emphysema. Isoflavone is a polyphenolic compound that exists in soybeans. Daidzein and genistein, two types of isoflavones, have been reported to have anti-inflammatory effects in various organs. We hypothesized that the daidzein-rich soy isoflavone aglycones (DRIAs) attenuate cigarette smoke-induced emphysema in mice. Mice were divided into four groups: the (i) control group, (ii) isoflavone group, (iii) smoking group, and (iv) isoflavone + smoking group. The number of inflammatory cells in the bronchoalveolar lavage fluid (BALF) and the airspace enlargement using the mean linear intercept (MLI) were determined 12 weeks after smoking exposure. Expressions of neutrophilic inflammatory cytokines and chemokines were also examined. In the isoflavone + smoking group, the number of neutrophils in BALF and MLI was significantly less than that in the smoking group. Furthermore, the gene-expressions of TNF-α and CXCL2 (MIP-2) in the isoflavone + smoking group were significantly less than those in the smoking group. Supplementation of the COPD murine model with DRIAs significantly attenuates pathological changes of COPD via suppression of neutrophilic inflammation. MDPI 2019-08-29 /pmc/articles/PMC6769447/ /pubmed/31470503 http://dx.doi.org/10.3390/nu11092023 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Kojima, Kazuya Asai, Kazuhisa Kubo, Hiroaki Sugitani, Arata Kyomoto, Yohkoh Okamoto, Atsuko Yamada, Kazuhiro Ijiri, Naoki Watanabe, Tetsuya Hirata, Kazuto Kawaguchi, Tomoya Isoflavone Aglycones Attenuate Cigarette Smoke-Induced Emphysema via Suppression of Neutrophilic Inflammation in a COPD Murine Model |
title | Isoflavone Aglycones Attenuate Cigarette Smoke-Induced Emphysema via Suppression of Neutrophilic Inflammation in a COPD Murine Model |
title_full | Isoflavone Aglycones Attenuate Cigarette Smoke-Induced Emphysema via Suppression of Neutrophilic Inflammation in a COPD Murine Model |
title_fullStr | Isoflavone Aglycones Attenuate Cigarette Smoke-Induced Emphysema via Suppression of Neutrophilic Inflammation in a COPD Murine Model |
title_full_unstemmed | Isoflavone Aglycones Attenuate Cigarette Smoke-Induced Emphysema via Suppression of Neutrophilic Inflammation in a COPD Murine Model |
title_short | Isoflavone Aglycones Attenuate Cigarette Smoke-Induced Emphysema via Suppression of Neutrophilic Inflammation in a COPD Murine Model |
title_sort | isoflavone aglycones attenuate cigarette smoke-induced emphysema via suppression of neutrophilic inflammation in a copd murine model |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6769447/ https://www.ncbi.nlm.nih.gov/pubmed/31470503 http://dx.doi.org/10.3390/nu11092023 |
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