To investigate whether TGF-β1/Smad2 signal pathway is involved in the process of apoptosis induced by seawater-induced acute lung injury.

A549 human lung cancer cells were cultured in vitro and treated with seawater at the concentrations of 20%, 40%, and 60%, respectively. According to the MTT results, the optimal concentration of seawater was selected for subsequent studies. The cells were pretreated with the inhibitor SB431542, and then treated with the optimal concentration of seawater. Then the expression level of apoptosis-related molecule cleaved caspase-3 was detected by Real-time PCR and Western blotting, and the cell apoptosis was observed by flow cytometry and Hoechst staining. At the same time, the expression levels of TGF-β1, Smad2 and p-Smad2 were detected by Real-time PCR and Western blotting.

As the concentration of seawater increased, the viability of A549 cells gradually decreased, and 40% of seawater was used for the subsequent research. Seawater treatment could cause obvious apoptosis of the cells, and the inhibitor SB431542 could significantly restore the level of apoptosis induced by seawater. At the same time, the expression level of TGF-β1 was significantly up-regulated by seawater, and the abnormal up-regulation was significantly decreased by the inhibitor. While the expression level of Smad2 was not significantly changed, but seawater can significantly up-regulate the expression level of p-Smad2, and the up-regulation of p-Smad2 can be significantly inhibited after the inhibitor treatment.

Seawater-induced acute lung injury may activate the TGF-β1/Smad2 signal pathway and regulate the activity of the apoptosis-executing protein Caspase-3, thereby promoting the apoptosis in the lung tissue cells.