简介：BackgroundNowadays,thestudiesmainlyfocusonthefunctionofdecreasingtheinflammatoryfactorandimprovingthefunctionsofendothelium,buttheeffectsofstatinsonventricularremodelingarerarelystudied.MethodsThe2-kindey,1-cliphypertensiverats(2K1C,Goldblatt)werepreparedwithSprague-Dawley(SD)rat.SDratswererandomlydividedintothreegroups:controlrats,hypertensiveratsandhypertensiveratstreatedwithatorvastatin(2mg·kg-1·d-1).After6weeks,systolicbloodpressure(SBP)wasmeasuredusingthetail-cuffmethod.TheplasmaconcentrationofangiotensinⅡandreninactivityweredeterminedbyradioimmunoassay.Theheartweight,theratioofleftventricularweightandbodyweightwascalculated.ResultsTheplasmaconcentrationofangiotensinⅡ(106.4±7.8)ng/Landreninactivity(20.6±2.4)ng/Lweresignificantlyincreaedinhypertensiveratscomparedwithnormalrats[(72.3±5.4)ng/Land(12.5±3.7)ng/L](P<0.01).Theheartweight(1.46±0.09)g,theratio3.54±0.19(×10-3)ofleftventricularweightandbodyweightinhypertensiveratswereobviouslyhigherthanthatinnormalrats[(0.98±0.07)gand(2.28±0.06)×10-3](P<0.01).Aftertreatmentwithatorvastatin,theplasmaconcentrationofangiotensinⅡ(68.3±6.9)ng/Landreninactivity(8.7±2.3)ng/L,heartweight(1.05±0.04)g,theratio2.36±0.07(×10-3)aboveweredecreasedsignificantly,therewerenodifferencebetweenthegroupofhypertensiveratsandthenormal.ConclusionsAtorvastatincandecreasetheratioofleftventricularweightandbodyweightandhastheeffectsoncardiovascularremodelinginhypertensiverats.

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：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.