Propofol Prevents Autophagic Cell Death following Oxygen and Glucose Deprivation in PC12 Cells and Cerebral Ischemia-Reperfusion Injury in Rats 英文参考文献.docVIP

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Propofol Prevents Autophagic Cell Death following Oxygen and Glucose Deprivation in PC12 Cells and Cerebral Ischemia-Reperfusion Injury in Rats 英文参考文献.doc

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Propofol Prevents Autophagic Cell Death following Oxygen and Glucose Deprivation in PC12 Cells and Cerebral Ischemia-Reperfusion Injury in Rats 英文参考文献

PropofolPreventsAutophagicCellDeathfollowing OxygenandGlucoseDeprivationinPC12Cellsand CerebralIschemia-ReperfusionInjuryinRats DerongCui1.,LiWang1.,AihuaQi2,QuanhongZhou1,XiaoliZhang1,WeiJiang1* 1DepartmentofAnesthesiology,ShanghaiSixthPeople’sHospitalAffiliatedwithShanghaiJiaotongUniversity,Shanghai,China,2DepartmentofPostgraduateSchool, SoochowUniversity,Suzhou,China Abstract Background:Propofolexertsprotectiveeffectsonneuronalcells,inpartthroughtheinhibitionofprogrammedcelldeath. Autophagic cell death is a type of programmed cell death that plays elusive roles in controlling neuronal damage and metabolichomeostasis.Wethereforestudiedwhetherpropofolcouldattenuatetheformationofautophagosomes,andif so,whethertheinhibitionofautophagiccelldeathmediatestheneuroprotectiveeffectsobservedwithpropofol. Methodology/PrincipalFindings:Thecellmodelwasestablishedbydeprivingthecellsofoxygenandglucose(OGD)for6 hours, and the rat model of ischemia was introduced by a transient two-vessel occlusion for 10 minutes. Transmission electronmicroscopy(TEM)revealedthattheformationofautophagosomesandautolysosomesinbothneuronalPC12cells andpyramidalrathippocampalneuronsafterrespectiveOGDandischemia/reperfusion(I/R)insults.Awesternblotanalysis revealedthattheautophagy-relatedproteins,suchasmicrotubule-associatedprotein1lightchain3(LC3-II),Beclin-1and classIIIPI3K,werealsoincreasedaccordingly,butcytoprotectiveBcl-2proteinwasdecreased.ThenegativeeffectsofOGD andI/R,includingtheformationofautophagosomesandautolysosomes,theincreaseinLC3-II,Beclin-1andclassIIIPI3K expressionandthedeclineinBcl-2productionwereallinhibitedbypropofolandspecificinhibitorsofautophagy,suchas3- methyladenine(3-MA),LY294002andBafilomycinA1(Baf),.Furthermore,invitroOGDculturesandinvivoI/Rratsshowed anincreaseincellsurvivalfollowingtheadministrationofpropofol,asassessedbyanMTTassayorhistochemicalanalyses. Conclusions/Significance:Ourdatasuggestthatpropofolcanmarkedlyattenuateautophagicprocessesviathedecreased expressiono