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1、作者简介:刘启亮,男,重庆铜梁县人,硕士研究生,医师,主要从事心血管疾病基础与临床方面的研究。电话:13370735316,E-mail:liuqiliangzy@sina.com通信作者:宋耀明,电话:(023)68755196,E-mail:ymsong@mail.xqhospital.com.cn收稿日期:2009-07-16;修回日期:2009-08-13Neuregulin-1β对阿霉素致心衰大鼠心肌细胞凋亡及bax、bcl-2蛋白表达的干预效应刘启亮,宋耀明,刘超(第三军医大学新桥医院心血管内科,全军心血管病研究所,重庆400037)摘要:目的观
2、察阿霉素所致心衰大鼠心肌细胞凋亡和bax、bcl-2蛋白表达情况及NRG-1β的干预作用。方法60只雄性SD大鼠200~250g,随机分成3组:阿霉素心肌病组(ADR-DCM,n=20),阿霉素2mg/kg,尾静脉注射,每周1次,连续注射8周;阿霉素心肌病+NRG-1治疗组(NRG,n=20),在注射ADR后8周后即开始给予nuregulin-1β10μgkg-1.d-1尾静脉注射,连续5d;正常对照组(CON,n=20),用2ml/kg生理盐水,尾静脉注射,连续8周;9周后取心肌行HE染色病理观察并用Tunel法观察心肌细胞凋亡及用免疫印迹法(Wester
3、nblot)检测baxbcl-2蛋白的表达。结果心肌细胞凋亡指数:模型组与NRG治疗组心肌细胞调亡指数较正常对照组显著增高(p<0.05),与模型组相比,NRG治疗组凋亡指数显著降低(p<0.05);bax、bcl-2蛋白表达:与模型组比较,NRG治疗组bcl-2蛋白表达明显上调(p<0.05),bax蛋白表达明显下调(p<0.05)。结论NRG-1β能够抑制阿霉素所致心衰大鼠心肌细胞凋亡,其机制可能与bcl-2蛋白表达上调,bax蛋白表达下调,bcl-2/bax值上调有关。关键词:neuregulin-1β心衰心肌凋亡baxbcl-2中图法分类号:文献标识
4、码:AEffectsofNeuregulin-1βonapoptosisandproteinexpressionsofbcl-2andbaxincardiomyocytesofadriamycin-inducedcardiomyopathyinratsLIUqi-liang,SONGyao-ming,LIUchao(CardiovascularDiseaseResearchCenter,XinqiaoHospital,ThirdMilitaryMedicalUniversity,Chongqing400037,China)Abstract:Objective
5、Tostudycardiomyocyteapoptosisandproteinexpressionsofbcl-2andbaxinadriamycin(ADM)-inducedmyocardialdamageinratstreatedwithnuregulin-1βMethodssixtymaleSDratsweighing200-250gwererandomlydividedintothreegroups:Control,ADR-DCMandADR+NRGgroups.ADR-DCMgroup(n=20):inwhich2.0mg/kgofadriamyc
6、in(ADR)wasweeklyinjectedviaatailveinfor8weeks;theADR+NRGgroup,concomitantNRG-1andADR(n=20),inwhich2.0mg/kgofadriamycin(ADR)wasweeklyinjectedviaatailveinfor8weeks,afterthatNRG-1nuregulin-1β10μgkg-1.d-1injectedviaatailveinfor5days;Controlgroup(n=20):ratsreceived2ml/kgnormalsalinebyin
7、jection,onceaweekfor8weeks.Nighweekslater,ratswereexecutedunderanesthesia,apoptoticcardiomyocytesweredetectedusingtheterminaldeoxynucleotidyltransferasemediateddUTPnickendlabeling(TUNEL)method.Theexpressionsofbcl-2andbaxproteinweredeterminedbywesternblot.ResultsTheindexofapoptoticc
8、ardiomyocytesincreasedsign