S-diclofenac Protects against Doxorubicin-Induced Cardiomyopathy in Mice via Ameliorating Cardiac Gap Junction Remodeling 英文参考文献.docVIP

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S-diclofenac Protects against Doxorubicin-Induced Cardiomyopathy in Mice via Ameliorating Cardiac Gap Junction Remodeling 英文参考文献.doc

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S-diclofenac Protects against Doxorubicin-Induced Cardiomyopathy in Mice via Ameliorating Cardiac Gap Junction Remodeling 英文参考文献

S-diclofenacProtectsagainstDoxorubicin-Induced CardiomyopathyinMiceviaAmelioratingCardiacGap JunctionRemodeling HuiliZhang1*,AlianZhang1,ChangfaGuo2,ChunzhiShi1,YangZhang1,QingLiu1,AnnaSparatore3, ChangqianWang1* 1Department of Cardiology, Shanghai Ninth People’s Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China, 2Department of Cardiac Surgery, ZhongshanHospital,FudanUniversity,Shanghai,China,3DipartimentodiScienzeFarmaceutiche‘‘PietroPratesi,’’Universita` degliStudidiMilano,Milano,Italy Abstract Hydrogen sulfide (H2S), as a novel gaseous mediator, plays important roles in mammalian cardiovascular tissues. In the presentstudy,weinvestigatedthecardioprotectiveeffectofS-diclofenac(2-[(2,6-dichlorophenyl)amino]benzeneaceticacid 4-(3H-1,2,dithiol-3-thione-5-yl)phenyl ester), a novel H2S-releasing derivative of diclofenac, in a murine model of doxorubicin-induced cardiomyopathy. After a single dose injection of doxorubicin (15mg/kg, i.p.), male C57BL/6J mice weregivendailytreatmentofS-diclofenac(25and50mmol/kg,i.p.),diclofenac(25and50mmol/kg,i.p.),NaHS(50mmol/kg, i.p.),orsamevolumeofvehicle.ThecardioprotectiveeffectofS-diclofenacwasobservedafter14days.ItshowedthatS- diclofenac,butnotdiclofenac,dose-dependentlyinhibitedthedoxorubicin-induceddownregulationofcardiacgapjunction proteins (connexin 43 and connexin 45) and thus reversed the remodeling of gap junctions in hearts. It also dose- dependently suppressed doxorubicin-induced activation of JNK in hearts. Furthermore, S-diclofenac produced a dose- dependent anti-inflammatory and anti-oxidative effect in this model. As a result, S-diclofenac significantly attenuated doxorubicin-related cardiac injury and cardiac dysfunction, and improved the survival rate of mice with doxorubicin- inducedcardiomyopathy.TheseeffectsofS-diclofenacweremimickedinlargepartbyNaHS.Therefore,weproposethat H2SreleasedfromS-diclofenacinvivocontributestotheprotectiveeffectindoxorubicin-inducedcardiomyopathy.These