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

Authors
  • Kim, Mun-Ock1
  • Lee, Jae-Won1
  • Lee, Jae Kyoung2
  • Song, Yu Na1, 3
  • Oh, Eun Sol1, 3
  • Ro, Hyunju3
  • Yoon, Dahye4
  • Jeong, Yun-Hwa1, 5
  • Park, Ji-Yoon1, 5
  • Hong, Sung-Tae5
  • Ryu, Hyung Won1
  • Lee, Su Ui1
  • Lee, Dae Young4
  • 1 Natural Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Cheongju 28116, Korea. , (North Korea)
  • 2 Rpbio Research Institute, Rpbio Co., Ltd., Suwon 16229, Korea. , (North Korea)
  • 3 Departments of Biological Sciences, College of Bioscience and Biotechnology, Chungnam National University, Daejeon 34134, Korea. , (North Korea)
  • 4 Department of Herbal Crop Research, National Institute of Horticultural and Herbal Science, Rural Development Administration, Eumseong 27709, Korea. , (North Korea)
  • 5 Departments of Anatomy & Cell Biology, Department of Medical Science, College of Medicine, Chungnam National University, Daejeon 35015, Korea. , (North Korea)
Type
Published Article
Journal
Antioxidants
Publisher
MDPI AG
Publication Date
Mar 30, 2022
Volume
11
Issue
4
Identifiers
DOI: 10.3390/antiox11040679
PMID: 35453364
Source
Medline
Keywords
Language
English
License
Unknown

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.

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