KMID : 0352720230470010081
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Journal of Ginseng Research 2023 Volume.47 No. 1 p.81 ~ p.88
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Respiratory protective effects of Korean Red Ginseng in a mouse model of particulate matter 4-induced airway inflammation
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Yang Won-Kyung
Kim Sung-Won Youn Soo-Hyun Hyun Sun-Hee Han Chang-Kyun Park Yang-Chun Lee Young-Cheol Kim Seung-Hyung
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Abstract
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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.
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KEYWORD
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Airway inflammation, Korean Red Ginseng, Korean Red Ginseng extract, Particulate matter, PM4+D-induced respiratory disease model 21
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