In conclusion, our study demonstrated the following: 1) sevoflurane preconditioning inhibited development of apoptosis in LPS-induced ALI; 2) sevoflurane-mediated anti-apoptotic activity was associated with decreased levels of caspase-3 and cleaved-caspase-3 and upregulation of Bcl-xl and Bcl-2; and 3) sevoflurane preconditioning is a potential therapeutic strategy to prevent lung injury resulting from aspiration events. This evidence concerns the gene BCL2L1 and acute respiratory distress syndrome.