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Respiratory protective effects of Korean Red Ginseng in a mouse model of particulate matter 4-induced airway inflammation

  • Won-Kyung, Yang (Division of Respiratory Medicine, Department of Internal Medicine, College of Korean Medicine, Daejeon University) ;
  • Sung-Won, Kim (Laboratory of Efficacy Research, Korea Ginseng Corporation) ;
  • Soo Hyun, Youn (Laboratory of Efficacy Research, Korea Ginseng Corporation) ;
  • Sun Hee, Hyun (Laboratory of Efficacy Research, Korea Ginseng Corporation) ;
  • Chang-Kyun, Han (Laboratory of Efficacy Research, Korea Ginseng Corporation) ;
  • Yang-Chun, Park (Division of Respiratory Medicine, Department of Internal Medicine, College of Korean Medicine, Daejeon University) ;
  • Young-Cheol, Lee (Department of Herbology, College of Korean Medicine, Sangji University) ;
  • Seung-Hyung, Kim (Institute of Traditional Medicine and Bioscience, Daejeon University)
  • Received : 2021.07.27
  • Accepted : 2022.05.23
  • Published : 2023.01.02

Abstract

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 ㎛) 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.

Keywords

Acknowledgement

This work was funded by KOREA GINSENG CORP.

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