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:ObjectivesTostudytheeffectoflatereperfusiononcaspase-3activityofischemicmyocardiuminrabbitanditssignificance.Methods24adultrabbitswererandomlydividedinto3groups:Sham(S)withoutligationofcoronaryartery,LateReperfusion(LR)withligationfor3hoursfollowingreleasefor3hoursandPersistentIschemia(PI)withpersistentligationofcoronaryarteryfor6hours.Allanimalsweresacrificed6hoursafterthebeginningoftheexperiments.BorderregionofinfarctedmyocardiumwereincisedforanalyzingtheconcentrationofSOD,MDA,GRandtheexpressionofFADD,Caspase-3andtheapoptosisindex(AI).ResultsComparedwiththeShamgroup,LRandPIgroupexhibitedmuchhigherMDA,FADD,Caspase-3,AIandmuchlowerSOD,GR(allP<0.01).ComparedwiththePIgroup,LRgroupexhibitedhigherMDA,FADD,Caspase-3,AIandlowerSOD,GR(allP<0.05).ConclusionsLatereperfusionmarkedlyenhancedtheCaspase-3activityandthenthenumberofapoptoticcardiomyocyteinborderregionofinfractedmyocardium,whichindicatedtheexistenceoflatereperfusioninjury.ThemechanismmayinvolvethehighoxidativestressstateandexpressionofFADD.
简介:BackgroundH9c2celllineismononucleatedmyoblastderivedfromembryonicrathearttissue.ActivitiesofTGF-β1,MMP-2andMMP-9increaseinH9c2cellsaftertreatmentwithfibrosisstimuli.MicroRNA(miRNA),akindofendogenoussmallnon-codingRNA,participatesincardiacfibrosis.Inthepresentstudy,expressionsoffibrosis-relatedgenesandmicroRNAsinTGF-β1treatedH9c2cellswereinvestigated.MethodsExpressionsoffibrosis-associatedgenes,includingCol3a1,α-SMA,FN1,CTGFandTSP-1,weremeasuredinTGF-β1treatedH9c2cellsbyquantitativereversetranscriptionandPCR(qRTPCR).Levelofα-SMAinH9c2cellswasdemonstratedbyfluorescenceimmunohistochemistry(FIHC)assay.ExpressionsofmaturemiR-16,-21a,-29binH9c2cellsweredeterminedbyqRT-PCRassay.ActivationsofSmad3andNF-kBsignalinginTGF-β1-treatedH9c2cellswerestudiedbydualluciferaseassay.ExpressionsofCol3a1,α-SMA,FN1,CTGFandTSP-1weredetectedinH9c2cellswithadenovirus-mediatedoverexpressionofmiR-21a.ResultsqRT-PCRassayshowedthatα-SMA,FN1,CTGF,TSP-1,butnotCol3a1,wereup-regulatedinTGF-β1treatedH9c2cells.FIHCresultalsorevealedthatα-SMAwasincreasedinTGF-β1-treatedH9c2cells.Consistently,dualluciferaseassayshowedthatSmad3andNF-kBsignalingproteinswereactivatedinTGF-β1-treatedH9c2cells.miR-21a,butnotmiR-16and-29b,wassignificantlyup-regulated.Additionally,over-expressionofmiR-21asignificantlyincreasesmRNAexpressionsofα-SMA,FN1,CTGFandTSP-1inH9c2cells.ConclusionsMiR-21aisup-regulatedinTGF-β1treatedH9c2cells,andmaycontributetoup-regulationsoffibrosis-associatedgenes.
简介:目的观察不同类型冠心病病人血清基质金属蛋白酶-9(matrixmetalloproteinase-9,MMP-9)、组织基质金属蛋白酶抑制物-1(tissue-inhibitorofmetalloproteinase-1,TIMP-1)和血管紧张素Ⅱ(anginotensinⅡ,AngⅡ)的血清浓度及相关关系,探讨急性冠状动脉综合征发病机制。方法冠心病病人分为急性心肌梗死组、不稳定心绞痛组(上述两组合称急性冠状动脉综合征组)和稳定心绞痛组,每组病人30例,另设健康对照组30例,比较各组间血清MMP-9、TIMP-1、MMP-9/TIMP-1和AngⅡ水平。结果急性心肌梗死组和不稳定心绞痛组血清MMP-9、MMP-9/TIMP-1和AngⅡ水平高于对照组,差异有统计学意义(P〈0.01),但稳定心绞痛组血清MMP-9、TIMP-1、MMP-9/TIMP-1和AngⅡ水平与对照组比较差异无统计学意义(P〉0.05),急性冠状动脉综合征组病人血清MMP-9、MMP-9/TIMP-1与AngⅡ水平呈正相关(P〈0.01)。结论血清MMP-9、MMP-9/TIMP-1和AngⅡ水平的增高与急性冠状动脉综合征相关,可作为评价冠状动脉粥样硬化斑块稳定性与病变严重程度的一个参考指标。
简介:甲状腺机能亢进(甲亢)合并病窦综合征较为少见,非常容易误诊,现将我院误诊3例报告如下.1.病例介绍例1:男,62岁.因心悸、胸闷2天伴多次晕厥於1996年9月5日入院.晕厥时四肢抽搐、小便失禁,约2分钟缓解.既往体健.入院体检:T36.8C、R21次/分、P83次/分、Bp113/79mmHg,无突眼,甲状腺未肿大,心界叩诊无扩大,HR86次/分,早搏15次/分,S1中等,未闻及病理性杂音,左肺少量湿性罗音,腹部、神经系统无殊.实验室检查:三大常规、肝肾功能、心肌酶学、电解质及血脂均正常,胸片示主动脉型心脏,心胸比例0.52,两肺纹理稍增粗,心电图示窦性心律、完全性右束支阻滞、频发房性早搏、短阵房速及房颤,反复窦性停搏,最长停搏8.2秒.
简介:目的探讨急性脑梗死患者血清基质金属蛋白酶-9(MMP-9)及外周白细胞(WBC)计数的变化。方法选择急性脑梗死患者124例(脑梗死组),分别测定其发病后24h内、5、14天的血清MMP-9、外周WBC,健康体检者40例(对照组),测空腹血清MMP-9和外周WBC,分析其与脑梗死面积的关系。结果脑梗死组与对照组比较,24h内血清MMP-9、WBC明显升高(P〈0.05),5天达高峰(P〈0.01),14天已明显下降,脑梗死组中大面积梗死表现最为明显;血清MMP-9、WBC有相关性,相关系数r=0.78(P〈0.01)。结论急性脑梗死患者血清MMP-9及外周WBC明显升高,并与病灶大小呈正比;MMP-9与WBC在动态变化中呈正相关。
简介:目的本研究旨在观察钙敏感受体(calcium-sensingreceptor,CaSR)在高糖诱导H9C2心肌细胞中的表达以及其对氧化应激的作用.方法将H9C2细胞在不同条件下干预24h,包括正常糖浓度组(NG组)、高糖组(HG组)、高糖+CaSR激动剂组(HG+GdCl3组)、高糖+CaSR抑制剂组(HG+NPS2390组).用CCK8试剂盒检测细胞存活率;DCFH-DA荧光探针检测细胞内活性氧簇(ROS)含量;用比色法检测细胞超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活性以及丙二醛(MDA)含量.用Westernblot检测细胞CaSR蛋白表达水平.结果细胞存活率呈糖浓度依赖性降低[(89.00±1.54)%比(98.83±0.47)%,P<0.01],CaSR蛋白表达量呈糖浓度依赖性增加2.14±0.09比1.06±0.05,P<0.01).高糖诱导可使细胞发生氧化应激,SOD(14.14±0.57比22.86±0.58,P<0.01)与GSH-Px(2.62±0.59比3.04±0.89,P<0.01)活性降低,ROS(0.040±0.002比0.020±0.001,P<0.01)与MDA(0.83±0.05比0.54±0.02,P<0.01)生成增多.与HG组相比,HG+GdCl3组细胞氧化损伤加重(P<0.05).而HG+NPS2390组细胞氧化损伤减轻(P<0.05).结论高糖能上调CaSR蛋白表达进而促进氧化应激的发生.