简介:ObjectivesToinvestigatethechangesofβ3-adrenoceptor(β3-AR)mRNAexpressionintheratswithchronicheartfailure(CHF),andtoexploretheeffectofβblockers(βBs)onβ3mRNAexpression.MethodsThirty-fourratswererandomlydividedintoShamgroup(n=10)andheartfailuregroup(n=24).Ratmodelwasestablishedbyaorticconstriction.Thesurvivalratsinheartfailuregroupweredividedintoheartfailurecontrolgroup(HFgroup,n=6),metoprololgroup(METgroup,n=8)andcarvedilolgroup(CARgroup,n=8)threemonthsafteroperation.Metoprololtartartewasstartedorallywith12mg·kg-1·d-1,carvedilolwith6mg·kg-1·d-1,isometricsalinewasstartedinHFgroup.Afterthreemonthsofdrugtherapy,measurementofhemodynamics,indexofventricularmass,thelevelofβ3-ARmRNAexpressionwereperformed.ResultsComparedwithShamgroup,leftventricularendsystolicpressure(LVESP),andtheabsolutevaluesofmaximalrateofriseandfall(±dp/dtmax)ofleftventricularpressurewereallsignificantlydecreased(P<0.01),leftventricularenddiastolicpressure(LVEDP)wassignificantlyincreasedinHFgroup(P<0.01).ThehemodynamicparameterswereimprovedbyβBs,andcarvedilolwasmoreeffectivethanmetoprolol(P<0.01).TheindexofventricularmasswashigherinHFgroupthanMETgroup,CARgroupandShamgroup(P<0.01).βBssignificantlydecreasedtheindexofleftventricularmass(LVMI),andCarvedilolwasmoreeffectivethanmetoprolol(P<0.01).Theindexofrightventricularmass(RVMI)didnotchangeinMETgroup(P>0.05),butsignificantdecreasecouldbeseeninCARgroup(P<0.01).Thelevelofβ3-ARexpressioninleftventriclewasgreaterthanthatinrightventriclewhetherinthefailingheartorinthenon-failingheart.ComparedwithShamgroup,thelevelofβ3-ARmRNAexpressionwassignificantlyincreasedinHFgroup(P<0.01).Thelevelsofβ3-ARmRNAexpressionshowedaremarkabledecreaseinCARgroup(P<
简介:目的探讨黄芪对实验性病毒性心肌炎细胞凋亡及Fas/FasL基因的影响.方法Balb/c小鼠24只腹腔感染柯萨奇病毒B3(CVB3)后随机分成2组:治疗组(每天腹腔注射黄芪注射液100mg/10g)及对照组.第8d取心脏标本,进行病理学检查、细胞凋亡TUNEL法检测以及逆转录聚合酶链反应(RT-PCR)分析Fas和FasLmRNA的表达水平.结果①黄芪治疗组病变积分明显低于对照组(P<0.01).②黄芪治疗组心肌细胞凋亡指数(AI)明显低于对照组(P<0.01).③黄芪治疗组心肌组织Fas和FasL的mRNA相对表达量均明显低于对照组(P<0.01,P<0.05).结论黄芪可通过下调病毒性心肌炎小鼠心肌组织Fas和FasL基因转录,减少心肌细胞凋亡和心肌损伤.
简介:目的研究心肌注射重组腺相关病毒(rAAV)2/1介导心肌肌浆网Ca2+-ATP酶(sERCA2a)基因治疗慢性心力衰竭犬的安全性。方法选取成年比格犬8只,随机分为对照组和SERCA2a基因转导组(转导组),每组4只。分别采用PCR、RTPCR和Westernblot法从DNA、RNA和蛋白水平检测rAAV2/1-rSERCA2a转导后在犬体内的分布;采用双夹心ELISA法检测转导组犬的血清。结果除注射rAAV2/1的心肌区域外,未注射rAAV2/1的心肌区域、主要脏器、骨骼肌和性腺中均未检测到rAAV2/1SERCA2a。对照组与转导组犬心肌、腰大肌、咀嚼肌和睾丸表现出相同的SERCA2a蛋白表达谱,未在其他组织中检测到。转导组犬血清内未检测到抗rAAV2/1抗体。结论rAAV2/1介导的基因转导是相对安全的,未整合到心脏以外的其他组织,也未在犬体内引发体液免疫。
简介:ObjectivesToexamineinvivointeractionsbetweenangiotensinⅡ(AngⅡ)AT1areceptor(AT1aR),angiotensin-convertingenzymes(ACE)andACE2usingsmallhairpinRNA(shRNA)gene-silencingmethodsinmicebrainstemnucleustractussolitarius(NTS).MethodsC57BLmice(n=8)wereusedasanimalmodel.MethodofmicroinjectioninthenucleusofNTSwasadopted.Aftertendays,micewerekilledandtheirbraintissuewerefixedandsectioned.TheexpressionlevelsofAT1aR,ACEandACE2mRNAatbothsidesofNTSwereexaminedbyinsituhybridization.Basedoncomparedt-test,thechangingformRNAexpressionwasexamined.ResultsAftertheexpressionofAT1aRmRNAwassignificantlyinhibited(61.6%±6.8%)byAT1aR-shRNA,itwasassociatedwithdecreasesinACE2mRNAexpressionfrom(1.05±0.12)μCi/mgto(0.74±0.09)μCi/mg(29.0%±14.5%,P<0.01)onthesamesideofthebrainstem.ACEmRNAexpressionwasconsistentatbothsides(0.50μCi/mg±0.09μCi/mgand0.53μCi/mg±0.08μCi/mg),withinsignificantdifference(P>0.05).ConclusionsThegenesilencingresultshowedthattherewereinteractionsbetweenbrainstemAT1aRandACE2.ACEmRNAexpressionwasnotalteredbyRNAinterferencetreatmentatAT1aR.
简介:ObjectivesToexamineeffectofatorvastatinontheexpressionofCOX-2inperipheralbloodmonocytesfrompatientswithearlystageofacutemyocardialinfarction(AMI)invitro,andtheIL-6concentrationinsupernatantwasalsoexamined.MethodsPatientswithAMI(n=40)andwithstablecoronaryheartdisease(CHD)(n=18)wereregistered.Peripheralbloodmonocytesfromallparticipantswereisolatedandculturedfor24hrs,butthosefrompatientswithAMIwererandomlyexposedtovariousconcentrationofatorvastatin(0,0.1,1,10μmol/L)duringthecultivation.COX-2mRNAexpressioninmonocyteswasanalyzedbyreversetranscriptionpolymerasechainreaction(RT-PCR).ConcentrationofIL-6insupernatantwasmeasuredbyenzyme-linkedimmunosorbentassay(ELISA).ResultsCOX-2expressionandIL-6secretionbyperipheralbloodmonocytesfrompatientswithAMI(0.92±0.13,205±46pg/ml)werehigherthanthatfromcontrols(0.19±0.08,41±8pg/ml)(bothP<0.05),andCOX-2expressionwasdramaticallyreducedupto52%byatorvastatin(P<0.05),inaconcentration-dependentmannerrespectively.TheexpressionofCOX-2frompatientswithAMIwasobviouslycorrelatedwiththesecretionofIL-6(r=0.636,P<0.05).COX-2expressioninthemonocytesafterinterventionofatorvastatinwasalsopositivelycorrelatedwithIL-6secretionbythesecells(r=0.783,P<0.05).ConclusionsCOX-2involvesinflammatoryrespondinearly-stageofAMI.AtorvastatinmaydecreaseCOX-2expressioninperipheralbloodmonocytesfrompatientswithAMIandcyclooxygenase-dependentpathwaymightbecorrelatedwiththeanti-inflammationmechanismofstatin.
简介:高血压是一种常见的疾病,在我国慢性非传染性疾病中位列第一,患病率仍在迅速上升,与此相对,我国人群高血压的知晓率、控制率和治疗率仍处于较差水平。
简介:目的观察缺血和再灌注不同时间大鼠海马不同区域神经营养因子-3(NT-3)mRNA表达的变化及其与神经元凋亡的关系.方法用Smi山法制备前脑缺血和再灌注大鼠模型;随机引物法标记NT-3cDNA探针;原位杂交检测NT-3mRNA表达情况;原位末端标记法检测凋亡神经元.结果前脑短暂缺血后,海马CAl、CA2、CA3区和齿状回NT-3mRNA表达均一过性下降,并随再灌注进一步加重,尤以CAl区下降幅度明显,且持续时间长,此后各区逐渐恢复正常水平;CA4区NT-3mRNA表达无显著性变化;各脑区、各时段NT-3mRNA表达水平与神经元凋亡呈显著负相关.结论前脑缺血和再灌注后,NT-3表达的减少可能是神经元凋亡的重要原因之一.
简介:ObjectivesToinvestigatetheeffectsofatorvastatinonthemRNAexpressionofintercellularadhesionmolecule-1(ICAM-1)andvascularcelladhesionmolecule-1(VCAM-1)activatedbyTNF-αinculturedhumanumbilicalveinendothelialcells(HUVEC).MethodsandResultsLacticdehydrogenase(LDH)activityintheculturemediaincreasedwhenHUVECwereincubatedwithTNF-α,suggestingacytotoxiceffectofTNF-αonHUVEC.ThemRNAexpressionofICAM-1andVCAM-1increasedinHUVECincubatedwith10μg/LTNF-αandreachedpeakinHUVECincubatedwith30μg/LTNF-α.ThemRNAexpressionofICAM-1andVCAM-1inHUVECincubatedwith30μg/LTNF-αbegantoincreaseat6h,reachedpeakat48h,andkeptaplateauuntil72h.Atorvastatindose-dependentlyinhibitedthemRNAexpressionsofICAM-1andVCAM-1activatedbyincubatingHUVECwith30μg/LTNF-αfor48hours.ConclusionsAtorvastatinmightstabilizeplaqueanddeceleratetheprocessofASbyinhibitingthemRNAexpressionsofICAM-1andVCAM-1.
简介:目的探讨与研究在小儿病毒性心肌炎临床治疗活动中应用抗病毒+黄芪注射液联合治疗方案的可行性以及其临床疗效。方法本研究选择46例患有病毒性心肌炎疾病患儿作为本次研究对象,这些病例患儿所选时间为2013年12月。2014年12月,并且将这些患儿随机分组为观察组与对照组。然后对观察组患儿以及对照组患儿分别给予抗病毒+黄芪注射液联合治疗方案、单纯抗病毒治疗方案,以对比两组患儿的临床疗效。结果在抗病毒+黄芪注射液联合治疗方案背景下的观察组患儿,其所获得的临床总有效率为95.7%,而在单纯抗病毒治疗方案背景下的对照组患儿,其所获得的临床总有效率为73.9%,差异具有统计学意义,P〈O.05。结论在小儿病毒性心肌炎临床治疗活动中,抗病毒+黄芪注射液联合治疗方案值得实施与推广。
简介:冠心病(cownaryheartdisease)又称缺血性心脏病,是一种严重危害人类健康的疾病,是由于冠状动脉粥样硬化造成血管痉挛,从而引起血管腔狭窄或阻塞,发生冠脉循环障碍,造成心肌缺血、缺氧甚至坏死的一种常见心脏病。目前,国内外公认的传统疗法有药物治疗、介入治疗(interventionaltherapy)及外科治疗,后者又包括冠状动脉旁路移植术(coronaryarterybypassgrafting)和心脏移植术(hearttransplantation)。然而药物治疗对病变严重的心肌缺血效果有限,而介入治疗和外科治疗后手术部位或冠状动脉其他部位可发生再狭窄,所以这三种治疗均不能根治冠心病。随着分子生物学理论和技术的进展,特别是在基因载体的构建、靶基因的界定和转基因技术等方面所取得的重要进展,使许多因基因结构或表达异常引起的心血管疾病利用基因治疗有望获得根治。