Epigallocatechin gallate improves airway inflammation through TGF‑β1 signaling pathway in asthmatic mice.

Abstract

The present study aimed to investigate the effect of epigallocatechin gallate (EGCG) on airway inflammation in mice with bronchial asthma, and the regulatory mechanism of transforming growth factor (TGF)-β1 signaling pathway, so as to provide theoretical basis for research and development of a novel drug for clinical treatment. Mouse models of bronchial asthma were established and injected with dexamethasone and EGCG via the caudal vein. 7 days later, bronchoalveolar tissue was collected for hematoxylin and eosin staining. Determination of airway resistance (AWR) and lung function in mice was detected. Serum was separated for cytometric bead array to detect the changes in inflammatory factors. Bronchoalveolar lavage fluid was collected for eosinophil and neutrophil counts. Fresh blood was obtained for flow cytometry to determine the percentages of Th17 and Treg cells. Bronchovesicular tissue was utilized for western blot assay and reverse transcription-quantitative polymerase chain reaction to determine the proteins and transcription factors in the TGF-β1 pathway. EGCG 20 mg/kg significantly reduced asthmatic symptoms, lung inflammatory cell infiltration, and the inflammatory factor levels of interleukin (IL)-2, IL-6 and tumor necrosis factor (TNF)-α. In addition, it increased the levels of inflammatory factors, including IL-10, diminished the percentage of Th17 cells, increased the percentage of Treg cells, and decreased the expression of TGF-β1 and phosphorylated (p)-Smad2/3 expression. Following the inhibition of the TGF-β1 receptor, the anti-inflammatory effect of EGCG disappeared, and the expression of TGF-β1 and p-Smad2/3 increased. EGCG attenuated airway inflammation in asthmatic mice, decreased the percentage of Th17 cells and increased the percentage of Treg cells. The anti-inflammatory effect of EGCG is achieved via the TGF-β1 signaling pathway.