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Artemisia argyi attenuates airway inflammation in lipopolysaccharide induced acute lung injury model
Artemisia argyi is used as a health supplement, tea, and food source in Korea. This study aimed to evaluate the effect of Artemisia argyi (AA) and its active compound, dehydromatricarin A (DA), on the attenuation of airway inflammation in a murine model of lipopolysaccharide (LPS)-induced acute lung...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Korean Association for Laboratory Animal Science
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5645598/ https://www.ncbi.nlm.nih.gov/pubmed/29046695 http://dx.doi.org/10.5625/lar.2017.33.3.209 |
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author | Shin, Na-Rae Park, Sung-Hyeuk Ko, Je-Won Ryu, Hyung-Won Jeong, Seong-Hun Kim, Jong-Choon Shin, Dong-Ho Lee, Hoon-Sang Shin, In-Sik |
author_facet | Shin, Na-Rae Park, Sung-Hyeuk Ko, Je-Won Ryu, Hyung-Won Jeong, Seong-Hun Kim, Jong-Choon Shin, Dong-Ho Lee, Hoon-Sang Shin, In-Sik |
author_sort | Shin, Na-Rae |
collection | PubMed |
description | Artemisia argyi is used as a health supplement, tea, and food source in Korea. This study aimed to evaluate the effect of Artemisia argyi (AA) and its active compound, dehydromatricarin A (DA), on the attenuation of airway inflammation in a murine model of lipopolysaccharide (LPS)-induced acute lung injury (ALI). The C57BL/6 mice were administered AA (50 mg/kg or 100 mg/kg) and DA (10 mg/kg or 20 mg/kg) by oral gavage from day 0 to 7 days and LPS treated by intranasal instillation 48 hours before the sacrifice. The treatment of AA and DA markedly decreased inflammatory cells in the bronchoalveolar lavage fluid (BALF) compared with that in ALI-induced mice, which was accompanied by a significant reduction in the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in BALF. Furthermore, the administration of AA and DA clearly decreased inducible nitric oxide synthase (iNOS) expression and nuclear factor kappa B (NF-κB) phosphorylation in comparison with that in the ALI-induced mice. The histological examination of the lung tissue revealed that the administration of AA and DA suppressed the inflammatory cell infiltration into the peribronchial and alveolar lesions induced by LPS instillation. Collectively, our results indicated that AA and DA effectively decreased the airway inflammatory response induced by LPS instillation. Therefore, AA and DA may offer a potential therapy for airway inflammatory disease. |
format | Online Article Text |
id | pubmed-5645598 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Korean Association for Laboratory Animal Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-56455982017-10-18 Artemisia argyi attenuates airway inflammation in lipopolysaccharide induced acute lung injury model Shin, Na-Rae Park, Sung-Hyeuk Ko, Je-Won Ryu, Hyung-Won Jeong, Seong-Hun Kim, Jong-Choon Shin, Dong-Ho Lee, Hoon-Sang Shin, In-Sik Lab Anim Res Original Article Artemisia argyi is used as a health supplement, tea, and food source in Korea. This study aimed to evaluate the effect of Artemisia argyi (AA) and its active compound, dehydromatricarin A (DA), on the attenuation of airway inflammation in a murine model of lipopolysaccharide (LPS)-induced acute lung injury (ALI). The C57BL/6 mice were administered AA (50 mg/kg or 100 mg/kg) and DA (10 mg/kg or 20 mg/kg) by oral gavage from day 0 to 7 days and LPS treated by intranasal instillation 48 hours before the sacrifice. The treatment of AA and DA markedly decreased inflammatory cells in the bronchoalveolar lavage fluid (BALF) compared with that in ALI-induced mice, which was accompanied by a significant reduction in the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 in BALF. Furthermore, the administration of AA and DA clearly decreased inducible nitric oxide synthase (iNOS) expression and nuclear factor kappa B (NF-κB) phosphorylation in comparison with that in the ALI-induced mice. The histological examination of the lung tissue revealed that the administration of AA and DA suppressed the inflammatory cell infiltration into the peribronchial and alveolar lesions induced by LPS instillation. Collectively, our results indicated that AA and DA effectively decreased the airway inflammatory response induced by LPS instillation. Therefore, AA and DA may offer a potential therapy for airway inflammatory disease. Korean Association for Laboratory Animal Science 2017-09 2017-09-27 /pmc/articles/PMC5645598/ /pubmed/29046695 http://dx.doi.org/10.5625/lar.2017.33.3.209 Text en Copyright © 2017 Korean Association for Laboratory Animal Science http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Shin, Na-Rae Park, Sung-Hyeuk Ko, Je-Won Ryu, Hyung-Won Jeong, Seong-Hun Kim, Jong-Choon Shin, Dong-Ho Lee, Hoon-Sang Shin, In-Sik Artemisia argyi attenuates airway inflammation in lipopolysaccharide induced acute lung injury model |
title | Artemisia argyi attenuates airway inflammation in lipopolysaccharide induced acute lung injury model |
title_full | Artemisia argyi attenuates airway inflammation in lipopolysaccharide induced acute lung injury model |
title_fullStr | Artemisia argyi attenuates airway inflammation in lipopolysaccharide induced acute lung injury model |
title_full_unstemmed | Artemisia argyi attenuates airway inflammation in lipopolysaccharide induced acute lung injury model |
title_short | Artemisia argyi attenuates airway inflammation in lipopolysaccharide induced acute lung injury model |
title_sort | artemisia argyi attenuates airway inflammation in lipopolysaccharide induced acute lung injury model |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5645598/ https://www.ncbi.nlm.nih.gov/pubmed/29046695 http://dx.doi.org/10.5625/lar.2017.33.3.209 |
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