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.