Cardioprotective Effects of 20(S)-Ginsenoside Rh2 against Doxorubicin-Induced Cardiotoxicity In Vitro and In Vivo英文文献资料.docVIP
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Cardioprotective Effects of 20(S)-Ginsenoside Rh2 against Doxorubicin-Induced Cardiotoxicity In Vitro and In Vivo英文文献资料
HindawiPublishingCorporation
Evidence-BasedComplementaryandAlternativeMedicine
Volume2012,ArticleID506214,8pages
doi:10.1155/2012/506214
ResearchArticle
CardioprotectiveEffectsof20(S)-GinsenosideRh2against
Doxorubicin-InducedCardiotoxicityInVitroandInVivo
HongboWang, PengfeiYu, HaitaoGou, JianqiaoZhang, MeiZhu, Zhen-huaWang,
1 1 2 1 1 2
Jing-weiTian,1,2Yong-taoJiang,1,2andFeng-huaFu1
1
2
DepartmentofPharmacology,SchoolofPharmacy,YantaiUniversity,Yantai264005,China
StateKeyLaboratoryofLong-ActingandTargetingDrugDeliveryTechnologies,LuyePharmaGroupLtd.,Yantai264003,China
CorrespondenceshouldbeaddressedtoFeng-huaFu,fufenghua@
Received27May2012;Revised23August2012;Accepted13September2012
AcademicEditor:Seung-HeonHong
Copyright?2012HongboWangetal.ThisisanopenaccessarticledistributedundertheCreativeCommonsAttributionLicense,
whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkisproperlycited.
Doxorubicin(DOX)isconsideredasoneofthebestantineoplasticagents.However,itsclinicaluseisrestrictedbyitsassociated
cardiotoxicity,whichismediatedbytheproductionofreactiveoxygenspecies.Inthisstudy,20(S)-ginsenosideRh2(Rh2)was
exploredwhetherithadprotectivee?ectsagainstDOX-inducedcardiotoxicity.Invitro studyonH9C2cellline,aswellasin
vivoinvestigationinonemouseandoneratmodelofDOX-inducedcardiomyopathy,wascarriedout.Theresultsshowedthat
pretreatmentwithRh2signi?cantlyincreasedtheviabilityofDOX-injuredH9C2cells.Inthemousemodel,Rh2couldsuppress
theDOX-inducedreleaseofthecardiacenzymesintoserumandimprovedtheoccurredpathologicalchangesthroughameliorating
thedecreasedantioxidantbiomoleculesandthecumulatedlipidperoxidationmalondialdehydeinhearttissues.Intheratmodel,
Rh2couldattenuatethechangeofECGresultingfromDOXadministration.Furthermore,Rh2enhancedtheantitumoractivity
ofDOXinA549cells.Our?ndingsthusdemonstratedthatRh2pretreatmentcoulde?ectivelyalleviateheartinjuryinducedby
DOX,andRh
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