Cargando…
Respiratory protective effects of Korean Red Ginseng in a mouse model of particulate matter 4-induced airway inflammation
BACKGROUND: Air pollution has led to an increased exposure of all living organisms to fine dust. Therefore, research efforts are being made to devise preventive and therapeutic remedies against fine dust-induced chronic diseases. METHODS: Research of the respiratory protective effects of KRG extract...
Autores principales: | , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2023
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9834024/ https://www.ncbi.nlm.nih.gov/pubmed/36644393 http://dx.doi.org/10.1016/j.jgr.2022.05.008 |
_version_ | 1784868368634871808 |
---|---|
author | Yang, Won-Kyung Kim, Sung-Won Youn, Soo Hyun Hyun, Sun Hee Han, Chang-Kyun Park, Yang-Chun Lee, Young-Cheol Kim, Seung-Hyung |
author_facet | Yang, Won-Kyung Kim, Sung-Won Youn, Soo Hyun Hyun, Sun Hee Han, Chang-Kyun Park, Yang-Chun Lee, Young-Cheol Kim, Seung-Hyung |
author_sort | Yang, Won-Kyung |
collection | PubMed |
description | BACKGROUND: Air pollution has led to an increased exposure of all living organisms to fine dust. Therefore, research efforts are being made to devise preventive and therapeutic remedies against fine dust-induced chronic diseases. METHODS: Research of the respiratory protective effects of KRG extract in a particulate matter (PM; aerodynamic diameter of <4 μm) plus diesel exhaust particle (DEP) (PM4+D)-induced airway inflammation model. Nitric oxide production, expression of pro-inflammatory mediators and cytokines, and IRAK-1, TAK-1, and MAPK pathways were examined in PM4-stimulated MH-S cells. BALB/c mice exposed to PM4+D mixture by intranasal tracheal injection three times a day for 12 days at 3 day intervals and KRGE were administered orally for 12 days. Histological of lung and trachea, and immune cell subtype analyses were performed. Expression of pro-inflammatory mediators and cytokines in bronchoalveolar lavage fluid (BALF) and lung were measured. Immunohistofluorescence staining for IRAK-1 localization in lung were also evaluated. RESULTS: KRGE inhibited the production of nitric oxide, the expression of pro-inflammatory mediators and cytokines, and expression and phosphorylation of all downstream factors of NF-κB, including IRAK-1 and MAPK/AP1 pathway in PM4-stimulated MH-S cells. KRGE suppressed inflammatory cell infiltration and number of immune cells, histopathologic damage, and inflammatory symptoms in the BALF and lungs induced by PM4+D; these included increased alveolar wall thickness, accumulation of collagen fibers, and TNF-α, MIP2, CXCL-1, IL-1α, and IL-17 cytokine release. Moreover, PM4 participates induce alveolar macrophage death and interleukin-1α release by associating with IRAK-1 localization was also potently inhibited by KRGE in the lungs of PM4+D-induced airway inflammation model. KRGE suppresses airway inflammatory responses, including granulocyte infiltration into the airway, by regulating the expression of chemokines and inflammatory cytokines via inhibition of IRAK-1 and MAPK pathway. Conclusion: Our results indicate the potential of KRGE to serve as an effective therapeutic agent against airway inflammation and respiratory diseases. |
format | Online Article Text |
id | pubmed-9834024 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-98340242023-01-13 Respiratory protective effects of Korean Red Ginseng in a mouse model of particulate matter 4-induced airway inflammation Yang, Won-Kyung Kim, Sung-Won Youn, Soo Hyun Hyun, Sun Hee Han, Chang-Kyun Park, Yang-Chun Lee, Young-Cheol Kim, Seung-Hyung J Ginseng Res Research Article BACKGROUND: Air pollution has led to an increased exposure of all living organisms to fine dust. Therefore, research efforts are being made to devise preventive and therapeutic remedies against fine dust-induced chronic diseases. METHODS: Research of the respiratory protective effects of KRG extract in a particulate matter (PM; aerodynamic diameter of <4 μm) plus diesel exhaust particle (DEP) (PM4+D)-induced airway inflammation model. Nitric oxide production, expression of pro-inflammatory mediators and cytokines, and IRAK-1, TAK-1, and MAPK pathways were examined in PM4-stimulated MH-S cells. BALB/c mice exposed to PM4+D mixture by intranasal tracheal injection three times a day for 12 days at 3 day intervals and KRGE were administered orally for 12 days. Histological of lung and trachea, and immune cell subtype analyses were performed. Expression of pro-inflammatory mediators and cytokines in bronchoalveolar lavage fluid (BALF) and lung were measured. Immunohistofluorescence staining for IRAK-1 localization in lung were also evaluated. RESULTS: KRGE inhibited the production of nitric oxide, the expression of pro-inflammatory mediators and cytokines, and expression and phosphorylation of all downstream factors of NF-κB, including IRAK-1 and MAPK/AP1 pathway in PM4-stimulated MH-S cells. KRGE suppressed inflammatory cell infiltration and number of immune cells, histopathologic damage, and inflammatory symptoms in the BALF and lungs induced by PM4+D; these included increased alveolar wall thickness, accumulation of collagen fibers, and TNF-α, MIP2, CXCL-1, IL-1α, and IL-17 cytokine release. Moreover, PM4 participates induce alveolar macrophage death and interleukin-1α release by associating with IRAK-1 localization was also potently inhibited by KRGE in the lungs of PM4+D-induced airway inflammation model. KRGE suppresses airway inflammatory responses, including granulocyte infiltration into the airway, by regulating the expression of chemokines and inflammatory cytokines via inhibition of IRAK-1 and MAPK pathway. Conclusion: Our results indicate the potential of KRGE to serve as an effective therapeutic agent against airway inflammation and respiratory diseases. Elsevier 2023-01 2022-06-14 /pmc/articles/PMC9834024/ /pubmed/36644393 http://dx.doi.org/10.1016/j.jgr.2022.05.008 Text en © 2022 The Korean Society of Ginseng. Publishing services by Elsevier B.V. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Research Article Yang, Won-Kyung Kim, Sung-Won Youn, Soo Hyun Hyun, Sun Hee Han, Chang-Kyun Park, Yang-Chun Lee, Young-Cheol Kim, Seung-Hyung Respiratory protective effects of Korean Red Ginseng in a mouse model of particulate matter 4-induced airway inflammation |
title | Respiratory protective effects of Korean Red Ginseng in a mouse model of particulate matter 4-induced airway inflammation |
title_full | Respiratory protective effects of Korean Red Ginseng in a mouse model of particulate matter 4-induced airway inflammation |
title_fullStr | Respiratory protective effects of Korean Red Ginseng in a mouse model of particulate matter 4-induced airway inflammation |
title_full_unstemmed | Respiratory protective effects of Korean Red Ginseng in a mouse model of particulate matter 4-induced airway inflammation |
title_short | Respiratory protective effects of Korean Red Ginseng in a mouse model of particulate matter 4-induced airway inflammation |
title_sort | respiratory protective effects of korean red ginseng in a mouse model of particulate matter 4-induced airway inflammation |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9834024/ https://www.ncbi.nlm.nih.gov/pubmed/36644393 http://dx.doi.org/10.1016/j.jgr.2022.05.008 |
work_keys_str_mv | AT yangwonkyung respiratoryprotectiveeffectsofkoreanredginsenginamousemodelofparticulatematter4inducedairwayinflammation AT kimsungwon respiratoryprotectiveeffectsofkoreanredginsenginamousemodelofparticulatematter4inducedairwayinflammation AT younsoohyun respiratoryprotectiveeffectsofkoreanredginsenginamousemodelofparticulatematter4inducedairwayinflammation AT hyunsunhee respiratoryprotectiveeffectsofkoreanredginsenginamousemodelofparticulatematter4inducedairwayinflammation AT hanchangkyun respiratoryprotectiveeffectsofkoreanredginsenginamousemodelofparticulatematter4inducedairwayinflammation AT parkyangchun respiratoryprotectiveeffectsofkoreanredginsenginamousemodelofparticulatematter4inducedairwayinflammation AT leeyoungcheol respiratoryprotectiveeffectsofkoreanredginsenginamousemodelofparticulatematter4inducedairwayinflammation AT kimseunghyung respiratoryprotectiveeffectsofkoreanredginsenginamousemodelofparticulatematter4inducedairwayinflammation |