Bufalin Induces Reactive Oxygen Species Dependent Bax Translocation and Apoptosis in ASTC-a-1 Cells英文文献资料.docVIP
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Bufalin Induces Reactive Oxygen Species Dependent Bax Translocation and Apoptosis in ASTC-a-1 Cells英文文献资料
HindawiPublishingCorporation
Evidence-BasedComplementaryandAlternativeMedicine
Volume2011,ArticleID249090,12pages
doi:10.1093/ecam/nep082
OriginalArticle
BufalinInducesReactiveOxygenSpeciesDependentBax
TranslocationandApoptosisinASTC-a-1Cells
LeiSun, TongshengChen, XiaopingWang, YunChen, andXunbinWei
1 1 2 3 3
1
MOEKeyLaboratoryofLaserLifeScienceInstituteofLaserLifeScience,SouthChinaNormalUniversity,
Guangzhou510631,China
2
3
DepartmentofAnesthesiology,TheFirstA?liatedHospitalofJinanUniversity,Guangzhou510632,China
InstitutesofBiomedicalSciences,FudanUniversity,Shanghai200032,China
CorrespondenceshouldbeaddressedtoTongshengChen,chentsh@
Received1February2009;Accepted15June2009
Copyright?2011LeiSunetal.ThisisanopenaccessarticledistributedundertheCreativeCommonsAttributionLicense,which
permitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkisproperlycited.
Bufalinhasbeenshowntoinducecancercelldeaththroughapoptoticpathways.However,themolecularmechanismsarenot
wellunderstood.Inthisstudy,weusedtheconfocal?uorescencemicroscopy(CFM)tomonitorthespatio-temporaldynamics
ofreactiveoxygenspecies(ROS)production,Baxtranslocationandcaspase-3activationduringbufalin-inducedapoptosisin
livinghumanlungadenocarcinoma(ASTC-a-1)cells.BufalininducedROSproductionandapoptoticcelldeath,demonstratedby
Hoechst33258stainingaswellas?owcytometryanalysis.Baxredistributedfromcytosoltomitochondriafrom12to48hafter
bufalintreatmentinlivingcellsexpressedwithgreen?uorescentproteinBax.TreatmentwiththeantioxidantN-acetyl-cysteine
(NAC),aROSscavenger,inhibitedROSgenerationandBaxtranslocationandledtoasigni?cantprotectionagainstbufalin-
inducedapoptosis.Ourresultsalsorevealedthatbufalininducedaprominentincreaseofcaspase-3activationblockedpotently
byNAC.Takentogether,bufalininducedROS-mediatedBaxtranslocation,mitochondrialpermeabilitytransitionandcaspase-3
activation,implyingthatbufalininducedapoptosisviaROS-depende
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