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时间:2020-03-08
《血红素加氧酶1在左心室肥厚和心力衰竭中的表达及其意义.doc》由会员上传分享,免费在线阅读,更多相关内容在工程资料-天天文库。
1、血红索加氧酶1在左心室肥厚和心力衰竭屮的表达及其意义[摘要]目的:探讨在左心室肥厚向心力衰竭的转变过程屮心肌细胞凋亡和血红素加氧酶1的表达及意义。方法:采用缩窄腹主动脉造成心力衰竭模型,术后分为3纟R,假手术纟R10只、心肌肥厚组10只和心力衰竭组10只。假手术组、心肌肥厚组于6周时处死,心力衰竭组于14周时处死,处死前行血流动力学、心肌肥厚检测,TUNEL法检测心肌细胞凋亡,WesternBlot法检测心肌Caspase-3和血红素加氧酶1的表达。结果:心力衰竭纽.较心肌肥厚组、假手术组心肌细胞凋亡增加(P<0.05),Caspa
2、se-3表达增加(P<0.01);心肌肥厚组较心力衰竭纟R、假手术组血红素加氧酶1表达增加(P〈0.05)。结论:心肌细胞凋亡在心脏由肥厚向衰竭的转变过程屮起重要的作用,与血红索加氧酶1的改变有关。[关键词]心室肥厚;心力衰竭;细胞凋亡;血红素加氧酶1[中图分类号]R541.61E文献标识码]A[文章编号11673-7210(2011)07(c)-027-02Expressionandsignificaneeofhemeoxygenase1incardiomyocytefromleftventricularhypertrophyto
3、heartfailureCHENLizhiDepartmentofPharmacy,theFirstPeople'sHospitalofGuiyangCounty,Hu'nanProvince,Guiyang424400,China[Abstract]Objective:Toobservetheroleandsignificantofapoptosisandhemeoxygenase1inthetransitionfromLeftventricularhypertrophy(LVH)toheartfailure(HF).Method
4、s:Pathologicalmodelsofheartfailurewereestablishedbyconstrictionofabdominalaortaofratspartly.Afteroperation,30ratsweredividedrandomlyinto3groups,sham-operateclgroup(n=l0),ventricularhypertrophygroup(n=10),heartfailuregroup(n二10).After6weeks,theratsofsham-operatedgroupan
5、dventricularhypertrophygroupwerekilled.After14weeks,theratsofheartfailuregroupwerekilled.Thehemodynamicparametersandventricularhypertrophywerestudied・ApoptosiswerestainedinsitubyusingTUNEL.Themonitoringofhemeoxygendse1andCaspase-3proteinofcardiomyocytewasdeterminedbywe
6、sternbiot.Results:Comparedwithsham-operatedgroupandventricularhypertrophygroup,cardiomyocyteapoptoticeventsandexpress!onofCapase-3wereincreasedinheartfailuregroup(P<0.05).Expressionofthehemeoxygenase1wasincreasedintheventricularhypertrophygroup(P<0.01),whereasthatofhem
7、eoxygenase1wasdecreasedinheartfailuregroupcomparedwithventricularhypertrophygroup(P<0.05).Conclusion:CarcliomyocyteapoptosisplayanimportsntroleinthetransitionfromventricularhypertrophytoheartfailureLVD.ThetransitionfromLVHtoLVDisrelatedtothechangesofhemeoxygenase1.[Key
8、words]Ventricularhypertrophy;Heartfailure;Apoptosis;Hemeoxygenase1氧化应激是造成心肌组织损伤的重要机制,应激反应在导致心肌细胞的损伤和死亡的同时,也诱导多种特殊基因表达
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