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KMID : 0352720230470010081
Journal of Ginseng Research
2023 Volume.47 No. 1 p.81 ~ p.88
Respiratory protective effects of Korean Red Ginseng in a mouse model of particulate matter 4-induced airway inflammation
Yang Won-Kyung

Kim Sung-Won
Youn Soo-Hyun
Hyun Sun-Hee
Han Chang-Kyun
Park Yang-Chun
Lee Young-Cheol
Kim Seung-Hyung
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 ¥ìm) 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-¥êB, 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-¥á, MIP2, CXCL-1, IL-1¥á, and IL-17 cytokine release. Moreover, PM4 participates induce alveolar macrophage death and interleukin-1¥á 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.
KEYWORD
Airway inflammation, Korean Red Ginseng, Korean Red Ginseng extract, Particulate matter, PM4+D-induced respiratory disease model 21
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