Anti-inflammatory effect of Gyeji-tang in a chronic obstructive pulmonary disease mouse model induced by cigarette smoke and lipopolysaccharide

Pharm Biol. 2022 Dec;60(1):2040-2048. doi: 10.1080/13880209.2022.2131841.

Abstract

Context: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung disease associated with respiratory symptoms and narrowing of airways. Gyeji-tang (GJT) is a traditional Asian medicine that has been used to relieve early-stage cold symptoms, headache, and chills.

Objective: We examined the effect and potential molecular action mechanism of GJT in a mouse model of COPD induced by cigarette smoke (CS) plus lipopolysaccharide (LPS).

Materials and methods: COPD was induced in C57BL/6J mice via daily exposure to CS for 1 h for 8 weeks and intranasal administration of LPS on weeks 1, 3, 5, and 7. GJT (100 or 200 mg/kg) or roflumilast (5 mg/kg) was administrated daily for the final 4 weeks of COPD induction.

Results: Administration of GJT significantly suppressed the CS/LPS-induced increases in: the numbers of total cells and macrophages in bronchoalveolar lavage fluid; the expression levels of tumour necrosis factor-α, interleukin (IL)-6, IL-1β, and IL-8; the activities (phosphorylation) of nuclear factor kappa B and signal transducer and activator of transcription 3; and the expression levels of the structural remodelling markers, transforming growth factor beta, matrix metallopeptidase (MMP)-7, and MMP-9.

Discussion and conclusions: These results demonstrate that GJT prevents the lung inflammation and airway remodelling induced by CS plus LPS exposure in mice, suggesting that GJT may have therapeutic potential for the treatment of COPD.

Keywords: COPD animal model; airway remodelling; inflammation.

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / therapeutic use
  • Cigarette Smoking*
  • Disease Models, Animal
  • Interleukin-8 / metabolism
  • Interleukin-8 / pharmacology
  • Interleukin-8 / therapeutic use
  • Lipopolysaccharides / toxicity
  • Lung
  • Matrix Metalloproteinase 9 / metabolism
  • Mice
  • Mice, Inbred C57BL
  • NF-kappa B / metabolism
  • Nicotiana
  • Pulmonary Disease, Chronic Obstructive* / chemically induced
  • STAT3 Transcription Factor / metabolism
  • Transforming Growth Factor beta / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Lipopolysaccharides
  • Tumor Necrosis Factor-alpha
  • STAT3 Transcription Factor
  • NF-kappa B
  • Matrix Metalloproteinase 9
  • Interleukin-8
  • Anti-Inflammatory Agents
  • Transforming Growth Factor beta

Grants and funding

This research was supported by the Korea Institute of Oriental Medicine under grant [numbers KSN2013220 and KSN2021220].