4.6 Article

Anti-Inflammatory and Anti-Airway Remodeling Activities of Jakyakgamcho-Tang in a Mouse Model of COPD

Journal

APPLIED SCIENCES-BASEL
Volume 12, Issue 17, Pages -

Publisher

MDPI
DOI: 10.3390/app12178646

Keywords

chronic obstructive pulmonary disease; cigarette smoke; Jakyakgamcho-tang; lipopolysaccharide

Funding

  1. Korea Institute of Oriental Medicine [KSN2013220, KSN2021220]
  2. National Research Council of Science & Technology (NST), Republic of Korea [KSN2021220, KSN2013220] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Jakyakgamcho-tang (JGT) has been found to prevent airway inflammation and remodeling caused by chronic obstructive pulmonary disease (COPD) in a mouse model. It reduces inflammatory cell count, expression levels of inflammatory factors, and inhibits the increase of related proteins.
Jakyakgamcho-tang (JGT) is used in oriental medicine to treat inflammation and allergy. Chronic obstructive pulmonary disease (COPD) causes respiratory inflammation, airway remodeling, and pulmonary emphysema. We examine the influence of JGT on COPD by using a mouse model. COPD was induced by inhalation of cigarette smoke (CS) and nasal administration of lipopolysaccharide (LPS). In comparison to COPD mice induced by CS and LPS, mice administered with JGT exhibited significantly lower amounts of inflammatory cells and reduced expression levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), IL-1 beta, and monocyte chemoattractant protein-1 (MCP-1) in bronchoalveolar lavage fluid (BALF) and lung tissue. The elevated concentrations of transforming growth factor-beta (TGF-beta), alpha-smooth muscle actin (alpha-SMA), and matrix metallopeptidase-9 (MMP-9) induced by CS and LPS were also inhibited by JGT treatment. Moreover, JGT suppressed CS and LPS-induced phosphorylation of nuclear factor kappa B (NF-kappa B), extracellular signal-regulated kinase1/2 (ERK1/2) and mitogen-activated protein kinases (p38 MAPKs). In a COPD mouse model, our results demonstrated that JGT prevented CS and LPS induced airway inflammation and remodeling.

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