Abstract
Background: Cigarette smoking is the leading cause of chronic obstructive pulmonary disease. (-)-Epigallocatechin-3-gallate (EGCG), the major catechins in Chinese green tea, has been studied for its anti-oxidative and anti-inflammatory properties in cell and animal models. In this study, we aimed to analyze the effects of EGCG on cigarette smoke (CS)-induced airway inflammation and mucus secretion in the CS-exposed rat model.Methods: Male Sprague-Dawley rats were randomly divided into either sham air (SA) or CS exposure. EGCG (50 mg/kg b.wt.) was given by oral gavage every other day in both SA and CS-exposed animals. Oxidative stress and inflammatory markers were determined in serum and/or bronchoalveolar lavage fluid by biochemical assays or ELISA. Lung morphological changes were examined by Periodic Acid-Schiff, Masson’s Trichrome staining and immunohistochemical analysis. Western blot analysis was performed to explore the effects of EGCG on epidermal growth factor receptor (EGFR)-mediated signaling pathway.Results: (-)-Epigallocatechin-3-gallate treatment attenuated CS-induced oxidative stress, lung cytokine-induced neutrophil chemoattractant-1 release and neutrophil recruitment. CS exposure caused an increase in the number of goblet cells in line with MUC5AC upregulation, and increased lung collagen deposition, which were alleviated in the presence of EGCG. In addition, CS-induced phosphorylation of EGFR in rat lung was abrogated by EGCG treatment.Conclusion: (-)-Epigallocatechin-3-gallate treatment ameliorated CS-induced oxidative stress and neutrophilic inflammation, as well as airway mucus production and collagen deposition in rats. The present findings suggest that EGCG has a therapeutic effect on chronic airway inflammation and abnormal airway mucus production probably via inhibition of EGFR signaling pathway.
Highlights
Chronic obstructive Pulmonary Disease (COPD) is a healthcare issue afflicting more than 600 million people worldwide, estimated to become the third leading cause of death by the year 2020 (Murray and Lopez, 2013)
We investigated the effects of EGCG on cigarette smoke (CS)-induced airway inflammation and mucus hypersecretion and the associated signaling pathway using a CS-exposed rat model
Cigarette smoke exposure reduced the serum total-antioxidant capacity (T-AOC) and the activities of antioxidant enzymes such as superoxide dismutase (SOD) and CAT (p < 0.01 for CS and SA groups, respectively), which was blocked by EGCG administration (T-AOC: p < 0.01; SOD: p < 0.001; and CAT: p < 0.05) (Figures 1C–E)
Summary
Chronic obstructive Pulmonary Disease (COPD) is a healthcare issue afflicting more than 600 million people worldwide, estimated to become the third leading cause of death by the year 2020 (Murray and Lopez, 2013). COPD, which is characterized by the development of irreversible airflow obstruction, is associated with chronic inflammation, leading to progressive decline in lung function (Ito and Barnes, 2009). Exposure to cigarette smoke (CS) is widely attributed to be the major cause of COPD, with accumulation of oxidant burden and airway mucus hypersecretion being pivotal in the pathogenesis of the disease (Macnee, 2007). In COPD, mucus hypersecretion has an important influence on small airways, which would further block the existing narrow and obstructed airways, leading to deterioration of lung function. Cigarette smoking is the leading cause of chronic obstructive pulmonary disease. We aimed to analyze the effects of EGCG on cigarette smoke (CS)-induced airway inflammation and mucus secretion in the CS-exposed rat model
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