Objective:Toexploretherelationshipbetweenneuronalapoptosisandhypoxiaortraumaticinjury.Methods:Ratneuronsprimarilyculturedinvitroweretreatedwithhypoxia(thehypoxiagroup)ortraumaticinjury(thetraumagroup).Theneuronalapoptosiswasevaluatedwithmicroscope,TUNEL(terminaldeoxynucleotidyltransferasemediatedx-dUTPnickendlabeling)staining,flowcytometry,agarosegetelectrophoresisandimmunohistochemistry.Results:Morphologicalchangesofapoptosisappearedinthetreatedneurons,andtheDNAfragmentationshowed“ladder”break.Theapoptoticindexwas10.8%inthehypoxiagroupand4.8%inthetraumagroup,whileitwasonly1.6%inthecontrolgroup.Theexpressionofapoptosis-associatedgenes(c-myc,fasandfasL)increased.Conclusions:Hypoxiaortraumaticinjurycaninduceneuronalapoptosis,anditsmolecularmechanismisprobablyrelatedtotheexpressionsofapoptosis-associatedgenes.
