Epigallocatechin-3-gallate suppresses alveolar epithelial cell apoptosis in seawater aspiration-induced acute lung injury via inhibiting STAT1-caspase-3/p21 associated pathway

The apoptosis of alveolar epithelial cells is important in seawater aspiration-induced acute lung injury (ALI). The present study aimed to investigate whether epigallocatechin-3-gallate (EGCG) is able to suppress apoptosis in alveolar epithelial cells in seawater aspiration-induced ALI in vivo and in vitro, and the possible mechanisms underlying it. The results indicated that seawater aspiration-induced ALI in rats is accompanied by increased apoptosis in lung tissue cells and the expression of apoptosis-associated proteins, caspase-3 and p21. EGCG pretreatment significantly ameliorated seawater aspiration-induced ALI. Furthermore, EGCG decreased seawater aspiration-induced apoptosis and the expression of caspase-3 and p21 in lung tissue cells. Seawater-challenged A549 cells experienced increased apoptosis and elevated levels of phosphorylated-signal transducer and activator of transcription 1 (P-STAT1). EGCG pretreatment of the cells resulted in significantly decreased seawater-induced apoptosis and lower levels of STAT1 and P-STAT1 in A549 cells. This suggests that EGCG suppresses alveolar epithelial cell apoptosis in seawater aspiration-induced ALI via inhibiting the STAT1-caspase-3/p21 associated pathway.