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

Authors :
Mun-Ock Kim
Jae-Won Lee
Jae Kyoung Lee
Yu Na Song
Eun Sol Oh
Hyunju Ro
Dahye Yoon
Yun-Hwa Jeong
Ji-Yoon Park
Sung-Tae Hong
Hyung Won Ryu
Su Ui Lee
Dae Young Lee
Source :
Antioxidants, Vol 11, Iss 4, p 679 (2022)
Publication Year :
2022
Publisher :
MDPI AG, 2022.

Abstract

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.

Details

Language :
English
ISSN :
20763921
Volume :
11
Issue :
4
Database :
Directory of Open Access Journals
Journal :
Antioxidants
Publication Type :
Academic Journal
Accession number :
edsdoj.287a571ff04e9e97b57b259c21fe92
Document Type :
article
Full Text :
https://doi.org/10.3390/antiox11040679