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

Figure 5

EG relieved EMT and oxidative stress in PM2.5-induced lung epithelial cells in an AKT-dependent manner. (a) Cell viability of lung epithelial cells treated with different concentrations of EG (). (b) Cell viability of PM2.5-induced lung epithelial cells treated with different concentrations of EG (). (c). Cell viability of PM2.5-induced lung epithelial cells treated with EG (20 μM) after AKT was overexpressed by adenovirus infection (). (d–e) Comparison of mRNA levels of EMT markers including E-Cadherin and α-SMA in the indicated groups (). vs. the indicated groups; ns: no significance.

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