Green tea extract ameliorates macrophage-driven emphysematous lesions in chronic obstructive pulmonary disease induced by cigarette smoke condensate.
Jin-Hwa KimJeong-Won KimChang-Yeop KimJi-Soo JeongJe-Won KoTae-Won KimPublished in: Phytotherapy research : PTR (2023)
Chronic obstructive pulmonary disease (COPD) is an important lung disease characterized by complicated symptoms including emphysema. We aimed to explore the mechanisms underlying the protective effect of green tea extract (GTE) on cigarette smoke condensate (CSC)-induced emphysema by demonstrating the reduction of macrophage-induced protease expression through GTE treatment in vivo and in vitro. Mice were intranasally administered 50 mg/kg CSC once a week for 4 weeks, and doses of 100 or 300 mg/kg GTE were administered orally once daily for 4 weeks. GTE significantly reduced macrophage counts in bronchoalveolar lavage fluid and emphysematous lesions in lung tissues in CSC-exposed mice. In addition, GTE suppressed CSC-induced extracellular signal-regulated kinase (ERK)/activator protein (AP)-1 phosphorylation followed by matrix metalloproteinases (MMP)-9 expression as revealed by western blotting, immunohistochemistry, and zymography in CSC-instilled mice. These underlying mechanisms related to reduced protease expression were confirmed in NCI-H292 cells stimulated by CSC. Taken together, GTE effectively inhibits macrophage-driven emphysematous lesions induced by CSC treatment, and these protective effects of GTE are closely related to the ERK/AP-1 signaling pathway, followed by a reduced protease/antiprotease imbalance. These results suggest that GTE can be used as a supplementary agent for the prevention of emphysema progression in COPD patients.
Keyphrases
- chronic obstructive pulmonary disease
- lung function
- signaling pathway
- poor prognosis
- diabetic rats
- adipose tissue
- high glucose
- induced apoptosis
- pi k akt
- high fat diet induced
- drug induced
- oxidative stress
- transcription factor
- type diabetes
- end stage renal disease
- cell proliferation
- gene expression
- clinical trial
- idiopathic pulmonary fibrosis
- cell cycle arrest
- metabolic syndrome
- prognostic factors
- cystic fibrosis
- immune response
- protein kinase
- air pollution
- epithelial mesenchymal transition
- insulin resistance
- long non coding rna
- patient reported outcomes
- cell death
- tyrosine kinase
- study protocol