Epigallocatechin-3-gallate inhibits inflammation and epithelial-mesenchymal transition through the PI3K/AKT pathway via upregulation of PTEN in asthma

Asthma is a chronic disease associated with hyper-responsiveness, obstruction and remodeling of the airways. Epithelial-mesenchymal transition (EMT) has an important role in these alterations and may account for the accumulation of subepithelial mesenchymal cells, thus contributing to airway hyperresponsiveness and remodeling. Epigallo-catechin-3-gallate (EGCG), which is a type of polyphenol, is the most potent ingredient in green tea, and exhibits antibacterial, antiviral, antioxidative, anticancer and chemopreventive activities. Recently, numerous studies have investigated the protective effects of EGCG against asthma and other lung diseases. In the present study, the role of EGCG in ovalbumin (OVA)-challenged asthmatic mice was determined. In addition, the inhibitory effects of EGCG against transforming growth factor (TGF)-1-induced EMT and migration of 16HBE cells, and the underlying mechanisms of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway, were investigated by immunofluorescence, Transwell, wound healing assay and western blot analysis, respectively. The results indicated that EGCG may suppress inflammation and inflammatory cell infiltration into the lungs of OVA-challenged asthmatic mice, and may also inhibit EMT via the PI3K/AKT signaling pathway through upregulating the expression of phosphatase and tensin homolog (PTEN) in vivo and in vitro. The present study also revealed the anti-migratory effects of EGCG in TGF-1-induced 16HBE cells, thus suggesting it may reduce airway remodeling. The present study provides a novel insight into understanding the protective effects of EGCG on airway remodeling in asthma, and indicates that EGCG may be useful as an adjuvant therapy for bronchial asthma.