简介：BackgroundMyocardialfibrosisplaysacriticalroleintheprocessofdiabeticcardiacremolding.MicroRNAs(miRNAs)areendogenous,smallnon-codingRNAsthatnegativelyregulategeneexpressionindiversebiologicalandpathologicalprocesses.However,therolesofmiRNAsinmyocardialfibrosishavenotbeenwellelucidated.Inthepresentstudy,miRNAsprofilesinthefibroticmyocardiumofdb/dbmiceandmiRNAsexpressioninTGF-β1-stimulatedmousecardiacmyofibroblastswasexamined.MethodsHeartfunctionof18-week-olddb/dbmiceanddb/mcontrolmicewasdetectedbyechocardiography.miRNAexpressionprofileindiabeticmyocardiumwasdetectedbymiRNAmicroarray.Quantitativereal-timePCRwasusedtodeterminetheexpressionoffibrosis-relatedgenesandmiRNAprecursorsofinterest.Westernblotwasusedtodetectthelevelsoffibrosis-relatedproteins,activatedSmad3andtotalSmad3.ResultsTheresultofechocardiographyshowedthatleftventricularsystolicanddiastolicfunctionwasimpairedin18-week-olddb/dbmicewithoutsignificantchangeofejectionfraction(EF)andfractionalshortening(FS).Fibrosis-relatedgenesexpressionwasupregulatedandtheamountofphosphorylatedSmad3wasincreasedsignificantlyinthediabeticmyocardium.miRNAsdysregulationwasshownindiabeticmyocardium,sixty-eightmiRNAs,includingmiR-208b,miR-29b,miR-26bandmiR-30e,wereincreasedovertwo-fold,meanwhile,sixty-twomiRNAsweredecreasedmorethantwo-foldinthemyocardiumofdb/dbmicecomparedtodb/mcontrols.InparallelwithasignificantupregulationofCol1a1,Col3a1andCTGFmiRNAexpression,miR-208b,miR-29b,miR-26bandmiR-30eprecursorswerealsoshowntobeupregulatedinTGF-β1-inducedC57bl/6mousecardiacmyofibroblasts.ConclusionsmicroRNAsweredysregulatedindiabeticmyocardium,withtheactivationofTGF-β/smad3pathway,contributingtodiabeticmyocardialfibrosis.

简介：ObjectivesLittleisknownaboutthemechanismofexercise-indueedangiogenieresponseinisehemicmyoeardium.Thisstudywasdesignedtoinvestigatetheeffeetsofexercisetrainingonexpressionofvaseularendothelialgrowthfaetorandangiogenesisininfarctedheart.MethodsFiftymaleFVBmiceweredividedintothreesubgroupstotestvariousresponsestoexercise,includingtimedependentresponseofangiogenicfactorstoexercisetraininginintactheart(n=10)andinfarctedheart(n=10),aswellasexercise-inducedangiogenieresponseinheartwithmyocardialinfarction(MI)(n=30).Themiceintheexercise-traininggroupswereallowedtoexercisedailyat1hourperdayfor7days.ResultsVEGFproteinexpressionwasup-regulatedbyexercisetrainingintimedependentfashioninmicewithMI.AngiogenesiswasevidentbyincreasedmyocardialmicrovesselsobservedbyPECAM-1immunohistoc-hemicalstaininginpost-MIexercisegroup(16.5±3.4)/0.4mm^2versuspost-MIsedentarymice(10±2.1)/0.4mm^2(P<0.05).Cellproliferationassessmentshowedsignificantlyhigher(P<0.05)numberofBrdUpositivecellsinpostMImiceinexerciseerouoasopposedtosedentarypostMImice.2%TTCstainingdisclosedaprofounddifferenceinthesizeofMI(18.25±2.93)%inexercisegroupvssedentarygroup(29.26±7.64)%(P<0.05).ConclusionsActivationandup-regulationofVEGFininfarctedmiceheartmaycontributestheangiogenicresponsetoexercisetrainingattheearlystageofmyocardialinfarction.Thisunderscorestheimpactofexerciseonangiogenesisinpostmyocardialinfarctionsetting.

简介：BackgroundAnimalmodelsofmyocardialinfarction(MI)havebeenwidelyusedtostudythepathologicalandphysiologicalchangesthatoccurinMI,andtoobjectivelyevaluatetheefficacyofnewtreatments.Theyareanimportanttoolinthisprocedure.However,themortalityrateofMIanimalmodelshassofarbeenhigherthaninreal-lifesituations.Theaimofthisstudywastoexploretheuseofamodifiedretrogradetractiontrachealintubation(MRTI)methodforincreasingthesuccessrateofMImodelsinrats.MethodsSixtymaleSprague-Dawleyratswereusedintheexperiment.UsingtheMRTImethodofartificialairwaygeneration,weestablishedtheMImodelbyligationoftheleftanteriordescendingbranchofthecoronaryartery.WeanalyzedtheeffectsofMRTI,theuseoflidocaine,operativedetails,nursingconsiderationsduringtheoperation,andpost-operativefactorsonthesuccessrateoftheMImodelinrats.ResultsThesuccessrateofgeneratinganMImodelinratscanbesignificantlyincreasedusingthefollowingmethods:1)SettinguptheartificialairwaythroughtheuseofMRTIbyusingasingle-lumencentralvenouscatheter;2)Selectingaligationsite2mmbelowthemidpointoftheconnectionbetweentheleftatrialappendageandthepulmonarycone;3)Addingadropoflidocainetothesurfaceofthehearttoslowdowntheheartrate,maketheoperationeasiertoperform,andpreventarrhythmiaspostoperatively;4)Clearingupairwaysecretionstimelybothintraandpostoperatively;5)Makingsurethatratsareinawarmstatebothintraandpostoperatively;6)Preventingwoundinfection.ConclusionsUseoftheMRTImethodcanquicklyestablishanartificialairwayinrats.Intraoperativeuseoflidocaine,selectingaprecisevascularligationsite,andappropriatecarebothintraandpostoperativelycanincreasethesuccessrateofMImodelgeneration.更多还原