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Black Ginseng Extract Suppresses Airway Inflammation Induced by Cigarette Smoke and Lipopolysaccharides In Vivo

Cigarette smoke (CS) is a risk factor that can induce airway enlargement, airway obstruction, and airway mucus hypersecretion. Although studies have shown that Korean black ginseng extract (BGE) has potent anti-inflammatory and antioxidant activities, the CS-induced inflammatory responses and molecu...

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Autores principales: Kim, Mun-Ock, Lee, Jae-Won, Lee, Jae Kyoung, Song, Yu Na, Oh, Eun Sol, Ro, Hyunju, Yoon, Dahye, Jeong, Yun-Hwa, Park, Ji-Yoon, Hong, Sung-Tae, Ryu, Hyung Won, Lee, Su Ui, Lee, Dae Young
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9025275/
https://www.ncbi.nlm.nih.gov/pubmed/35453364
http://dx.doi.org/10.3390/antiox11040679
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author Kim, Mun-Ock
Lee, Jae-Won
Lee, Jae Kyoung
Song, Yu Na
Oh, Eun Sol
Ro, Hyunju
Yoon, Dahye
Jeong, Yun-Hwa
Park, Ji-Yoon
Hong, Sung-Tae
Ryu, Hyung Won
Lee, Su Ui
Lee, Dae Young
author_facet Kim, Mun-Ock
Lee, Jae-Won
Lee, Jae Kyoung
Song, Yu Na
Oh, Eun Sol
Ro, Hyunju
Yoon, Dahye
Jeong, Yun-Hwa
Park, Ji-Yoon
Hong, Sung-Tae
Ryu, Hyung Won
Lee, Su Ui
Lee, Dae Young
author_sort Kim, Mun-Ock
collection PubMed
description Cigarette smoke (CS) is a risk factor that can induce airway enlargement, airway obstruction, and airway mucus hypersecretion. Although studies have shown that Korean black ginseng extract (BGE) has potent anti-inflammatory and antioxidant activities, the CS-induced inflammatory responses and molecular mechanisms are yet to be examined. The aim of this study was to examine the effect of BGE on the airway inflammatory response and its molecular mechanisms, using CS/lipopolysaccharides (LPS)-exposed animals and PMA-stimulated human airway epithelial NCI-H292 cells. The results show that BGE inhibited the recruitment of immune cells and the release of inflammatory mediators, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, monocyte chemoattractant protein (MCP)-1, elastase, and reactive oxygen species (ROS) in the airways of CS/LPS-exposed animals. BGE inhibited mucus secretion and the expression of Mucin 5AC (MUC5AC). Furthermore, BGE exhibited an anti-inflammatory effect by downregulating a signaling pathway mediated by transforming growth factor-β-activated kinase (TAK) 1, an important protein that accelerates inflammation by cigarette smoke (CS). Overall, the findings show that BGE inhibits lung inflammation and mucus secretion by decreasing the activation of TAK1 both in human epithelial cells and in CS/LPS-exposed animals, and could be a potential adjuvant in the treatment and prevention of airway inflammatory diseases caused by airway irritants such as CS.
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spelling pubmed-90252752022-04-23 Black Ginseng Extract Suppresses Airway Inflammation Induced by Cigarette Smoke and Lipopolysaccharides In Vivo Kim, Mun-Ock Lee, Jae-Won Lee, Jae Kyoung Song, Yu Na Oh, Eun Sol Ro, Hyunju Yoon, Dahye Jeong, Yun-Hwa Park, Ji-Yoon Hong, Sung-Tae Ryu, Hyung Won Lee, Su Ui Lee, Dae Young Antioxidants (Basel) Article Cigarette smoke (CS) is a risk factor that can induce airway enlargement, airway obstruction, and airway mucus hypersecretion. Although studies have shown that Korean black ginseng extract (BGE) has potent anti-inflammatory and antioxidant activities, the CS-induced inflammatory responses and molecular mechanisms are yet to be examined. The aim of this study was to examine the effect of BGE on the airway inflammatory response and its molecular mechanisms, using CS/lipopolysaccharides (LPS)-exposed animals and PMA-stimulated human airway epithelial NCI-H292 cells. The results show that BGE inhibited the recruitment of immune cells and the release of inflammatory mediators, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, monocyte chemoattractant protein (MCP)-1, elastase, and reactive oxygen species (ROS) in the airways of CS/LPS-exposed animals. BGE inhibited mucus secretion and the expression of Mucin 5AC (MUC5AC). Furthermore, BGE exhibited an anti-inflammatory effect by downregulating a signaling pathway mediated by transforming growth factor-β-activated kinase (TAK) 1, an important protein that accelerates inflammation by cigarette smoke (CS). Overall, the findings show that BGE inhibits lung inflammation and mucus secretion by decreasing the activation of TAK1 both in human epithelial cells and in CS/LPS-exposed animals, and could be a potential adjuvant in the treatment and prevention of airway inflammatory diseases caused by airway irritants such as CS. MDPI 2022-03-30 /pmc/articles/PMC9025275/ /pubmed/35453364 http://dx.doi.org/10.3390/antiox11040679 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Kim, Mun-Ock
Lee, Jae-Won
Lee, Jae Kyoung
Song, Yu Na
Oh, Eun Sol
Ro, Hyunju
Yoon, Dahye
Jeong, Yun-Hwa
Park, Ji-Yoon
Hong, Sung-Tae
Ryu, Hyung Won
Lee, Su Ui
Lee, Dae Young
Black Ginseng Extract Suppresses Airway Inflammation Induced by Cigarette Smoke and Lipopolysaccharides In Vivo
title Black Ginseng Extract Suppresses Airway Inflammation Induced by Cigarette Smoke and Lipopolysaccharides In Vivo
title_full Black Ginseng Extract Suppresses Airway Inflammation Induced by Cigarette Smoke and Lipopolysaccharides In Vivo
title_fullStr Black Ginseng Extract Suppresses Airway Inflammation Induced by Cigarette Smoke and Lipopolysaccharides In Vivo
title_full_unstemmed Black Ginseng Extract Suppresses Airway Inflammation Induced by Cigarette Smoke and Lipopolysaccharides In Vivo
title_short Black Ginseng Extract Suppresses Airway Inflammation Induced by Cigarette Smoke and Lipopolysaccharides In Vivo
title_sort black ginseng extract suppresses airway inflammation induced by cigarette smoke and lipopolysaccharides in vivo
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9025275/
https://www.ncbi.nlm.nih.gov/pubmed/35453364
http://dx.doi.org/10.3390/antiox11040679
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