Epigallocatechin Gallate Relieved PM2.5‐Induced Lung Fibrosis by Inhibiting Oxidative Damage and Epithelial‐Mesenchymal Transition through AKT/mTOR Pathway

Oxidative damage and epithelial‐mesenchymal transition (EMT) are main pathological processes leading to the development of PM2.5‐induced lung fibrosis. Epigallocatechin gallate (EG), a natural polyphenol extracted from green tea, possesses the ability to combat oxidative stress and inflammation. However, the potential roles of EG in PM2.5‐induced lung fibrosis have not been reported yet. In the present study, we investigated whether EG could relieve PM2.5‐induced lung injury and fibrosis in vivo and in vitro. To mimic PM2.5‐induced lung fibrosis, C57/BL6 mice were intranasally instilled with PM2.5 suspension, and MLE‐12 lung epithelial cells were stimulated with PM2.5 (100 μg/mL) in vitro. The results showed that intragastric administration of EG (20 mg/kg/d or 80 mg/kg/d for 8 weeks) significantly prevented lung injury, inflammation, and oxidative stress in PM2.5‐induced mice, apart from inhibiting collagen deposition. Additionally, EG treatment also suppressed the activation of AKT/mTOR signaling pathway in lung tissues challenged with PM2.5. In vitro experiments further demonstrated that EG treatment could enhance cell viability in a concentration‐dependent manner in PM2.5‐treated MLE‐12 lung epithelial cells. Also, the overexpression of constitutively active AKT could offset the inhibitory effects of EG on EMT and oxidative stress in PM2.5‐treated MLE‐12 lung epithelial cells. Finally, AKT overexpression also blocked the inhibitory effect of EG on the phosphorylation of mTOR in PM2.5‐treated MLE‐12 lung epithelial cells. In conclusion, EG could improve PM2.5‐induced lung fibrosis by decreasing oxidative damage and EMT through AKT/mTOR pathway, which might be a potential candidate for the treatment of PM2.5‐induced lung fibrosis.