Analysisofanti-atheroscleroticroleofcarvedilolPapertowritenetwork:[Abstract]ObjectiveToinvestigatetheactivationoftheantioxidanteffectsofcarvedilolinatheroscleroticlesionsandproliferatingcellnuclearantigen(PCNAandnuclearfactorkappaBp65(NFκBp65.OfmaleNewZealandwhiterabbits24wererandomlydividedthenormalgroup,high-fatgroup,carvedilolcarvedilolgroup(n=8),foratotaldietfor10weeksaftertheendoftheexperiment,enzymaticdetectionofserumtriglycerideandcholesterolinrabbits,xanthineoxidaseserumultra-superoxidedismutase(SOD,thiobarbituricacidcolorimetricassayofmalondialdehyde(MDA,andthemethodofimmunohistochemicaldeterminationoftheexpressionofthevascularwallofPCNAandNFκBp65resultsofhigh-fatgroupandthecarvedilolgroupserumtriglycerideandcholesterolthanthenormalgroupwassignificantlyincreased(F=146.25,287.83,q=14.76~20.75,P<0.01,thedifferencebetweenthetwogroupswasnotstatisticallysignificant(q=0.53,0.59,P>0.05.fat1groupthaninthenormalgroup,SODsignificantlyreduced,MDAincreasedsignificantly,whileinthecarvedilolgroupahigherfat,SODwasincreased,MDAdecreased(F=21.65,75.64,q=4.98~24.29,P<0.01)..high-fatgroupPCNAandNFκBp65inexpressionsignificantlyincreasedcomparedwithnormalgroup,thecarvedilolgroupofPCNAandNFκBp65expressionofthehigherfatgroupwassignificantlyreduced(F=426.12,521.38,q=56.15~75.87,P<0.01.PCNANFκBp65thepositivecorrelation(r=0.975,P<0.01.ConclusionCarvedilolreducethelipidoxidativedamagemaybetheblockingofNFκBactivation,therebyinhibitingtheproliferationofsmoothmusclecells.[Keywords:]arteriosclerosiscarvedilolantioxidantcellproliferationinrabbit[ABSTRACT]ObjectiveTostudytheeffectofcarvedilolonantioxidationandactivationofPCANandNFκBonatherosclerosis.MethodsTwentyfourmaleNewZealandwhiterabbitswererandomlydividedintothreegroups:normalgroup,highfatdietgroupandcavediloltreatedgroup,witheightrabbitsineachgroup.Alltherabbitswerefedfor10weeks.After2completionoftheexperiment,thelevelsofserumtriglycerideandcholesterolweremeasuredbyenzymaticmethod,ofserumSODbyxanthineoxidativetechnique,andofserumMDAbythiobarbituricacidmethod.ExpressionofthePCANandNFκBp65inthevascularwallwasdetectedimmunohistochemically.ResultsComparedwiththoseofnormalrabbits,thelevelsofserumtriglycerideandcholesterolofthehighfatdietandcavediloltreatedwereextremelyhigh(F=146.25,287.83;q=14.76-20.75;P<0.01),butnostatisticaldifferencewasfoundbetweenthelattertwogroups(q=0.53,0.59;P>0.05).LowlevelserumSODandhighlevelserumMDAwerenoticedinhighfatdietrabbits.Inhighfatdietgroup,SODwaslowerthanthatinnormalgroup,andMDAwashigher;incavediloltreatedgroup,SODwashigher,andMDAwaslowerascomparedwithnormalgroup(F=21.65,75.64;q=4.98-24.29;P<0.01.TheexpressionofPCNAandNFκBp65inhighfatdietgroupwasmarkedlyincreasedascomparedwiththenormalgroup;buttheexpressionwasdecreasedincarvedilolgroupascomparedwithhighfatdiet(F=426.12,521.38;q=56.15-75.87,P<0.01.Ananalysisshowedthata3positivecorrelationexistedbetweenPCNAandNFκBp65.ConclusionCarvedilolmightrelievethelipidperoxidationinjuryandblockNFκBactivationsoastoinhibittheproliferationofsmoothmusclecells.[KEYWORDS]atherosclerosis;carvedilol;antioxidants;cellproliferation;rabbitsAtherosclerosis(AS)isthebasicpathologicalmanifestationsofmanycardiovascularandcerebrovasculardiseases,butalsooneofthecommondiseasesoftheelderlyseriousthreattohumanhealth.OxidativedamageistheASlesionincoreareas,andsmoothmusclecellmigr...