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

Won-Kyung Yang; Sung-Won Kim; Soo Hyun Youn; Sun Hee Hyun; Chang-Kyun Han; Yang-Chun Park; Young-Cheol Lee; Seung-Hyung Kim

doi:10.1016/j.jgr.2022.05.008

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

J Ginseng Res. 2023 Jan;47(1):81-88. doi: 10.1016/j.jgr.2022.05.008. Epub 2022 Jun 14.

Authors

Won-Kyung Yang^{1

2}, Sung-Won Kim³, Soo Hyun Youn³, Sun Hee Hyun³, Chang-Kyun Han³, Yang-Chun Park¹, Young-Cheol Lee⁴, Seung-Hyung Kim²

Affiliations

¹ Division of Respiratory Medicine, Department of Internal Medicine, College of Korean Medicine, Daejeon University, Daejeon, Republic of Korea.
² Institute of Traditional Medicine and Bioscience, Daejeon University, Daejeon, Republic of Korea.
³ Laboratory of Efficacy Research, Korea Ginseng Corporation, Daejeon, Republic of Korea.
⁴ Department of Herbology, College of Korean Medicine, Sangji University, Wonju, Republic of Korea.

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 μm) 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: Airway inflammation; Korean Red Ginseng; Korean Red Ginseng extract; PM4+D-induced respiratory disease model 21; Particulate matter.