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Treatment with eucalyptol mitigates cigarette smoke-induced lung injury through suppressing ICAM-1 gene expression
The present study was conducted to investigate the clinical significance of Eucalyptol in treating cigarette smoke-induced lung injury with the potential mechanism involved in the event. Rats were exposed to air (control) and cigarette smoke (smoking) after they were treated with Eucalyptol (260 mg/...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6435500/ https://www.ncbi.nlm.nih.gov/pubmed/29789401 http://dx.doi.org/10.1042/BSR20171636 |
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author | Yu, Na Sun, Yi-Tian Su, Xin-Ming He, Miao Dai, Bing Kang, Jian |
author_facet | Yu, Na Sun, Yi-Tian Su, Xin-Ming He, Miao Dai, Bing Kang, Jian |
author_sort | Yu, Na |
collection | PubMed |
description | The present study was conducted to investigate the clinical significance of Eucalyptol in treating cigarette smoke-induced lung injury with the potential mechanism involved in the event. Rats were exposed to air (control) and cigarette smoke (smoking) after they were treated with Eucalyptol (260 mg/kg) orally once a day for 12 weeks. Cell counts of bronchoalveolar lavage fluid (BALF), measurements of mean liner intercept (MLI) and mean alveolar number (MAN), and lung function test were executed in experimental animals. Contents of cytokines and intercellular adhesion molecule (ICAM)-1 in BALF and ICAM-1 protein and mRNA expression in lung tissues were determined by ELISA, immunohistochemistry (IHC), and RT-PCR, respectively. A rat model of chronic obstructive pulmonary disease (COPD) displayed declining lung function, increased cell counts and cytokine production in BALF, and emphysema-like lesions in cigarette smoke-exposed lungs compared with the controls (all P<0.01). Treatment with Eucalyptol partly reversed lung function decline with obvious decrease in inflammatory cell infiltrate, TNF-α, IL-6, and ICAM-1 expression levels in the challenged lungs (all P<0.05 and 0.01). Furthermore, oral administration of the drug not only reduced the emphysema-associated lung lesions but also suppressed ICAM-1 protein and mRNA expression in the lungs compared with the control (all P<0.05 or 0.01). Intervention of Eucalyptol mitigates the ongoing inflammatory process in airways and ameliorates the cigarette smoke-induced lung injury through suppressing ICAM-1 gene expression in the diseased lungs. |
format | Online Article Text |
id | pubmed-6435500 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-64355002019-04-12 Treatment with eucalyptol mitigates cigarette smoke-induced lung injury through suppressing ICAM-1 gene expression Yu, Na Sun, Yi-Tian Su, Xin-Ming He, Miao Dai, Bing Kang, Jian Biosci Rep Research Articles The present study was conducted to investigate the clinical significance of Eucalyptol in treating cigarette smoke-induced lung injury with the potential mechanism involved in the event. Rats were exposed to air (control) and cigarette smoke (smoking) after they were treated with Eucalyptol (260 mg/kg) orally once a day for 12 weeks. Cell counts of bronchoalveolar lavage fluid (BALF), measurements of mean liner intercept (MLI) and mean alveolar number (MAN), and lung function test were executed in experimental animals. Contents of cytokines and intercellular adhesion molecule (ICAM)-1 in BALF and ICAM-1 protein and mRNA expression in lung tissues were determined by ELISA, immunohistochemistry (IHC), and RT-PCR, respectively. A rat model of chronic obstructive pulmonary disease (COPD) displayed declining lung function, increased cell counts and cytokine production in BALF, and emphysema-like lesions in cigarette smoke-exposed lungs compared with the controls (all P<0.01). Treatment with Eucalyptol partly reversed lung function decline with obvious decrease in inflammatory cell infiltrate, TNF-α, IL-6, and ICAM-1 expression levels in the challenged lungs (all P<0.05 and 0.01). Furthermore, oral administration of the drug not only reduced the emphysema-associated lung lesions but also suppressed ICAM-1 protein and mRNA expression in the lungs compared with the control (all P<0.05 or 0.01). Intervention of Eucalyptol mitigates the ongoing inflammatory process in airways and ameliorates the cigarette smoke-induced lung injury through suppressing ICAM-1 gene expression in the diseased lungs. Portland Press Ltd. 2018-07-06 /pmc/articles/PMC6435500/ /pubmed/29789401 http://dx.doi.org/10.1042/BSR20171636 Text en © 2018 The Author(s). http://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (http://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research Articles Yu, Na Sun, Yi-Tian Su, Xin-Ming He, Miao Dai, Bing Kang, Jian Treatment with eucalyptol mitigates cigarette smoke-induced lung injury through suppressing ICAM-1 gene expression |
title | Treatment with eucalyptol mitigates cigarette smoke-induced lung injury through suppressing ICAM-1 gene expression |
title_full | Treatment with eucalyptol mitigates cigarette smoke-induced lung injury through suppressing ICAM-1 gene expression |
title_fullStr | Treatment with eucalyptol mitigates cigarette smoke-induced lung injury through suppressing ICAM-1 gene expression |
title_full_unstemmed | Treatment with eucalyptol mitigates cigarette smoke-induced lung injury through suppressing ICAM-1 gene expression |
title_short | Treatment with eucalyptol mitigates cigarette smoke-induced lung injury through suppressing ICAM-1 gene expression |
title_sort | treatment with eucalyptol mitigates cigarette smoke-induced lung injury through suppressing icam-1 gene expression |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6435500/ https://www.ncbi.nlm.nih.gov/pubmed/29789401 http://dx.doi.org/10.1042/BSR20171636 |
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