Black ginseng extract suppresses airway inflammation induced by cigarette smoke and lipopolysaccharides in vivo

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dc.contributor.authorMun-Ock Kim-
dc.contributor.authorJae-Won Lee-
dc.contributor.authorJ K Lee-
dc.contributor.authorYu Na Song-
dc.contributor.authorEun Sol Oh-
dc.contributor.authorH Ro-
dc.contributor.authorD Yoon-
dc.contributor.authorYun Hwa Jeong-
dc.contributor.authorJi-Yoon Park-
dc.contributor.authorS T Hong-
dc.contributor.authorHyung Won Ryu-
dc.contributor.authorSu Ui Lee-
dc.contributor.authorD Y Lee-
dc.date.accessioned2022-04-19T15:31:44Z-
dc.date.available2022-04-19T15:31:44Z-
dc.date.issued2022-
dc.identifier.issn2076-3921-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/25784-
dc.description.abstractCigarette smoke (CS) is a risk factor that can induce airway enlargement, airway obstruc-tion, 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.-
dc.publisherMDPI-
dc.titleBlack ginseng extract suppresses airway inflammation induced by cigarette smoke and lipopolysaccharides in vivo-
dc.title.alternativeBlack ginseng extract suppresses airway inflammation induced by cigarette smoke and lipopolysaccharides in vivo-
dc.typeArticle-
dc.citation.titleAntioxidants-
dc.citation.number4-
dc.citation.endPage679-
dc.citation.startPage679-
dc.citation.volume11-
dc.contributor.affiliatedAuthorMun-Ock Kim-
dc.contributor.affiliatedAuthorJae-Won Lee-
dc.contributor.affiliatedAuthorYu Na Song-
dc.contributor.affiliatedAuthorEun Sol Oh-
dc.contributor.affiliatedAuthorYun Hwa Jeong-
dc.contributor.affiliatedAuthorJi-Yoon Park-
dc.contributor.affiliatedAuthorHyung Won Ryu-
dc.contributor.affiliatedAuthorSu Ui Lee-
dc.contributor.alternativeName김문옥-
dc.contributor.alternativeName이재원-
dc.contributor.alternativeName이재경-
dc.contributor.alternativeName송유나-
dc.contributor.alternativeName오은솔-
dc.contributor.alternativeName노현주-
dc.contributor.alternativeName윤다혜-
dc.contributor.alternativeName정윤화-
dc.contributor.alternativeName박지윤-
dc.contributor.alternativeName홍성태-
dc.contributor.alternativeName류형원-
dc.contributor.alternativeName이수의-
dc.contributor.alternativeName이대영-
dc.identifier.bibliographicCitationAntioxidants, vol. 11, no. 4, pp. 679-679-
dc.identifier.doi10.3390/antiox11040679-
dc.subject.keywordAirway inflammation-
dc.subject.keywordBlack ginseng-
dc.subject.keywordCigarette smoke-
dc.subject.keywordMucin 5AC-
dc.subject.keywordReactive oxygen species-
dc.subject.localAirway Inflammation-
dc.subject.localAirway inflammation-
dc.subject.localairway inflammation-
dc.subject.localBlack ginseng-
dc.subject.localCigarette smoke-
dc.subject.localcigarette smoke-
dc.subject.localMucin 5AC-
dc.subject.localROS-
dc.subject.localReactive Oxygen Species (ROS)-
dc.subject.localReactive oxidative species-
dc.subject.localReactive oxygen species-
dc.subject.localReactive oxygen species (ROS)-
dc.subject.localreactive oxygen species-
dc.subject.localreactive oxygen species (ROS)-
dc.subject.localReactive Oxygen Species-
dc.subject.localReactive oxygen species(ROS)-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Natural Product Research Center > 1. Journal Articles
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