简介：Objective:Toobservehumanneuronalapoptosissecondarytotraumaticbraininjury,andtoelucidateitsregulativemechanismandthechangeofexpressionofapoptosis-relatedgenes.Methods:Specimensofbrainwerecollectedfromcasesoftraumaticbraininjuryinhumans.Thehistologicalandcellularmorphologywasexaminedbylightandelectronmicroscopy.TheextentofDNAinjurytocorticalneuronswasdetectedbyusingTUNEL.ByinsituhybridisationandimmunohistochemistrythemRNAchangesandproteinexpressionofBcl-2,Bax,p53,andcaspase3p20subunitwereobserved.Results:Apoptoticneuronsappearedfollowingtraumaticbraininjury,peakedat24hoursandlastedfor7days.Innormalbraintissueactivatedcaspase3wasrare,butashorttimeaftertraumaitbecameactivated.Theactivitypeakedat20-28hoursandremainedhigherthannormalfor5-7days.TherewasnoexpressionofBcl-2mRNAandBcl-2proteininnormalbraintissuebut8hoursafterinjurytheirexpressionbecameevidentandthenincreased,peakedat2-3daysandremainedhigherthannormalfor5-7days.TheprimaryexpressionofBax-mRNAandBaxproteinwashighinnormalbraintissue.At20-28hourstheyincreasedandremainedhighfor2-3days;onthe7thdaystheyreturnedtoanormallevel.Innormalbraintissue,p53mRNAandP53wereminimallyexpressed.Increasedexpressionwasdetectedatthe8thhour,anddecreasedat20-28hoursbutstillremainedhigherthannormalonthe5thday.Conclusions:Followingtraumaticinjurytothehumanbrain,apoptoticneuronsappeararoundthefocusoftrauma.ThemRNAandproteinexpressionofBcl-2,Baxandp53andtheactivityofcaspase3enzymeareincreased.