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《右丙亚胺对表柔比星致大鼠心肌损伤的保护作用及机制研究-论文.pdf》由会员上传分享,免费在线阅读,更多相关内容在应用文档-天天文库。
1、——40——肿瘤药学2014年2月第4卷第1期Anti—tumorPharmacy,February2014,Vo1.4,No.1《右丙亚胺对表柔比星致大鼠心肌损伤的保护作用及机制研究★吴晖,欧阳取长,刘莉萍,鲁军,水峥嵘(湖南省肿瘤医院/中南大学湘雅医学院附属肿瘤医院乳腺内科,湖南长沙,410013)摘要:目的探讨右丙亚胺对表柔比星致大鼠心肌损伤的保护作用及其机制,为临床用药提供实验依据。方法将35只SD大鼠随机分为5组:正常对照组、模型组(表柔比星+生理盐水)、表柔比星+低剂量右丙亚胺组(DEX1)、表柔比星+中剂量右丙亚胺组(DEX2)、表柔比星+高剂量右丙亚胺组(D
2、EX3),给药后检测各组大鼠心肌组织微量丙二醛(MDA)含量、总超氧化物歧化酶(T—SOD)活性和血浆乳酸脱氢酶(LDH)水平并观察心肌细胞凋亡的情况。结果与正常对照组比较,模型组大鼠心肌组织的SOD活性明显降低,MDA含量、血浆LDH含量和心肌细胞凋亡指数均明显升高(P<0.01);而与模型组比较,用右丙亚胺处理的各组大鼠心肌组织SOD活性明显升高,心肌组织MDA含量、心肌细胞凋亡指数及血浆LDH含量均显著降低(P3、毒性;细胞凋亡中图分类号:R979.1;R541.6文献标识码:A文章编号:2095—1264(2014)m一0040—06doi:10.39690.issn.2095—1264.2014.008EfectsofDexrazoxaneonPharmorubicinInducedMyocardialDamageanditsMechanisms★WUHui,OUYANGQuehang*,LIULiping,LUJun,SHUIZhengrong(Sre~tCancerTreatmentCentre,theAffiliatedTumorHospitalofXiangyaMedic4、alSchoolofCentralSouth矾—vers~Changsha,Hunan,410013,China)Abstract:ObjectiveToexploretheeffectsofdexrazoxaneonpharmorubicininducedmyocardialdamageanditsmecha—nisms.Methods35SDratswererandomlydividedintofivegroups:controlgroup,modelgroup(epirubicin+saline);DEX1group(epirubicin+lowdoseofdexra5、zoxane);DEX2group(epirubicin+mediumdoseofdexrazoxane);DEX3group(epirubicin+highdoseofdexrazoxane).Afteradministration,wedetectedthema1ondialdehyde(MDA)contentandtotalsuperoxidedismutase(T-SOD)activityinmyocardialtissues,plasmalactatedehydrogenase(LDH)levelsofeachgroup,andobservedcardiomyoc6、yteapoptosisinallgroups.ResultsComparedwiththecontrolgroup,theSODactivityinmyocardialtissueofmodelgroupwassig-nificanflydecreased,andtheMDAcontentinmyocardialtissue,theplasmaLDHcontent,andmyocardialcellapoptoticindexweresignificantlyincreased(P<0.01).Comparedwiththemodelgroup,theSODactivit7、yinmyocardialtissueofratstreatedbydifferentdosesofdexrazoxanewasmarkedlyincreased,andtheMDAcontentinmyocardialtissue,theplasmaLDHcontent,andmyocardialcellapoptoticindexweresignificantlydecreasedfP<0.01orP<0.05).ConclusionDexrazoxanecouldrelievepharmorubiein—in
3、毒性;细胞凋亡中图分类号:R979.1;R541.6文献标识码:A文章编号:2095—1264(2014)m一0040—06doi:10.39690.issn.2095—1264.2014.008EfectsofDexrazoxaneonPharmorubicinInducedMyocardialDamageanditsMechanisms★WUHui,OUYANGQuehang*,LIULiping,LUJun,SHUIZhengrong(Sre~tCancerTreatmentCentre,theAffiliatedTumorHospitalofXiangyaMedic
4、alSchoolofCentralSouth矾—vers~Changsha,Hunan,410013,China)Abstract:ObjectiveToexploretheeffectsofdexrazoxaneonpharmorubicininducedmyocardialdamageanditsmecha—nisms.Methods35SDratswererandomlydividedintofivegroups:controlgroup,modelgroup(epirubicin+saline);DEX1group(epirubicin+lowdoseofdexra
5、zoxane);DEX2group(epirubicin+mediumdoseofdexrazoxane);DEX3group(epirubicin+highdoseofdexrazoxane).Afteradministration,wedetectedthema1ondialdehyde(MDA)contentandtotalsuperoxidedismutase(T-SOD)activityinmyocardialtissues,plasmalactatedehydrogenase(LDH)levelsofeachgroup,andobservedcardiomyoc
6、yteapoptosisinallgroups.ResultsComparedwiththecontrolgroup,theSODactivityinmyocardialtissueofmodelgroupwassig-nificanflydecreased,andtheMDAcontentinmyocardialtissue,theplasmaLDHcontent,andmyocardialcellapoptoticindexweresignificantlyincreased(P<0.01).Comparedwiththemodelgroup,theSODactivit
7、yinmyocardialtissueofratstreatedbydifferentdosesofdexrazoxanewasmarkedlyincreased,andtheMDAcontentinmyocardialtissue,theplasmaLDHcontent,andmyocardialcellapoptoticindexweresignificantlydecreasedfP<0.01orP<0.05).ConclusionDexrazoxanecouldrelievepharmorubiein—in
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