Background:　Hyperbaric　oxygen　(HBO)　improves　skin　flap　function　and　inhibits　partial　necrosis　induced　by　ischemia-reperfusion　(I/R)　injury.　Our　study　aimed　to　evaluate　the　mechanism　underlying　HBO　regulation　of　the　antiapoptosis　factors　associated　with　I/R　injury　of　skin　flaps.　Methods:　The　rats　were　divided　into　sham　surgery,　I/R,　and　HBO　groups.　Rats　from　the　HBO　group　received　HBO　preconditioning　followed　by　I/R　surgery.　Blood　perfusion　of　the　skin　flaps　was　measured　with　laser　Doppler　flowmeters.　Tissue　morphology　and　apoptosis　were　subsequently　assessed　based　on　hematoxylin-eosinhe　and　terminal　deoxynucleotidyl　transferase　dUTP　nick-end　labeling　staining.　Protein　expression　of　phosphorylated　apoptosis　signal-regulating　kinase　1　(pASK-1),　phosphorylated　c-Jun　N-terminal　kinase　(pJNK),　B-cell　lymphoma-2　(Bcl-2),　and　Bcl2-associated　X　protein　(Bax)　was　examined　by　immunodetection,　and　Bcl-2　messenger　RNA　expression　was　detected　by　quantitative　polymerase　chain　reaction.　In　addition,　caspase-3　activity　was　also　measured.　Results:　The　result　of　microcirculation　analysis　showed　that　the　survival　and　blood　perfusion　rates　significantly　increased　in　the　skin　flap　after　HBO　exposure.　Terminal　deoxynucleotidyl　transferase　dUTP　nick-end　labeling　staining　revealed　that　cell　apoptosis　was　significantly　attenuated　in　the　HBO　group.　Furthermore,　HBO　preconditioning　increased　the　expression　of　Bcl-2　and　inhibited　pASK-1,　pJNK,　and　Bax　expression　as　determined　by　both　immunohistochemistry　and　Western　blot.　Caspase-3　activity　and　the　Bax/Bcl-2　ratio　declined　in　the　HBO　group.　Conclusions:　HBO　preconditioning　effectively　ameliorates　I/R　injury　by　regulating　the　apoptosis　signal-regulating　kinase　1　and/or　c-Jun　N-terminal　kinase　pathway　and　anti-and　proapoptosis　factors.　(C)　2015　Elsevier　Inc.　All　rights　reserved.