Details

Autor(en) / Beteiligte

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

Titel

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

Ist Teil von

• Journal of ginseng research, 2023-01, Vol.47 (1), p.81-88

Ort / Verlag

Korea (South): Elsevier B.V

Erscheinungsjahr

2023

Link zum Volltext

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• 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. 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. 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. Immunohistofluorescence (IHF) staining for IRAK1, CD11b, MCP-1, and TNF-α protein expression in lung tissues of a PM4+D-induced airway inflammation murine model. (A) IHF staining for IRAK1 (A-red), CD11b (A-green), merge (A-orange), Densitometric quantification of (B) IRAK1, (C) CD11b, (D) IHF staining for MCP-1 (D-red), and TNF-α (F-red) in lung tissues. Densitometric quantification of (E) MCP-1, and (G) TNF-α. Data are expressed as the mean ± SEM. BALB/c normal, PM4+D-sensitized control mice, 3 mg/kg dexamethasone-treated PM4+D-sensitized mice, 300 mg/kg KRGE-treated PM4+D-sensitized mice, 150 mg/kg KRGE-treated PM4+D-sensitized mice, and 75 mg/kg KRGE-treated PM4+D-sensitized mice. [Display omitted]