Background　and　objective　Blast　lung　injury　is　a　common　type　of　blast　injury　and　has　very　high　mortality.　Therefore,　research　to　identify　medical　therapies　for　blast　injury　is　important.　Perfluorocarbon　(PFC)　is　used　to　improve　gas　exchange　in　diseased　lungs　and　has　antiinflammatory　functions　in　vitro　and　in　vivo.　The　aim　of　this　study　was　to　determine　whether　PFC　reduces　damage　to　A549　cells　caused　by　blast　injury　and　to　elucidate　its　possible　mechanisms　of　action.　Study　design　and　methods　A549　alveolar　epithelial　cells　exposed　to　blast　waves　were　treated　with　and　without　PFC.　Morphological　changes　and　apoptosis　of　A549　cells　were　recorded.　PCR　and　enzymelinked　immunosorbent　assay　(ELISA)　were　used　to　measure　the　mRNA　or　protein　levels　of　IL-1　beta,　IL-6　and　TNF-alpha.　Malondialdehyde　(MDA)　levels　and　superoxide　dismutase　(SOD)　activity　levels　were　detected.　Western　blot　was　used　to　quantify　the　expression　of　NF-kappa　B,　Bax,　Bcl-2,　cleaved　caspase-3　and　MAPK　cell　signaling　proteins.　Results　A549　cells　exposed　to　blast　wave　shrank,　with　less　cell-cell　contact.　The　morphological　change　of　A549　cells　exposed　to　blast　waves　were　alleviated　by　PFC.　PFC　significantly　inhibited　the　apoptosis　of　A549　cells　exposed　to　blast　waves.　IL-1　beta,　IL-6　and　TNF-alpha　cytokine　and　mRNA　expression　levels　were　significantly　inhibited　by　PFC.　PFC　significantly　increased　MDA　levels　and　decreased　SOD　activity　levels.　Further　studies　indicated　that　NF-kappa　B,　Bax,　caspase-3,　phospho-p38,　phosphor-ERK　and　phosphor-JNK　proteins　were　also　suppressed　by　PFC.　The　quantity　of　Bcl-2　protein　was　increased　by　PFC.