Abstract: [
Abstract ] Objective Toexploretheeffectofcelecoxibontherelationshipbetweentumor
necrosisfactor-α ( TNF-α ) andapoptosisinpressureoverloadinducedmyocardialhypertrophyin
rat.Methods Male Wisterratsweredividedintosham2weeksgroup , sham4weeksgroup ,
model2weeksgroup , model4weeksgroup , modelpluscelecoxib2weeksgroupandmodelplus
celecoxib4weeksgroupinrandomizedorder.Theanimalmodelwasestablishedbyconstriction
ofabdominalaorta.Leftventriculartissuesectionswereobservedunderlightmicroscope.The
contentsofinflammatorycytokines TNF-αinplasmaandtissue wereexaminedby ELISA.
TUNELmethodwasperformedtodetecttheapoptosisofleftventricularmyocardialcells.Results
①Leftventricle HEstainingshowedthatthe myocardialcellhypertrophyandshapewere
irregular , myocardialhypertrophy wassignificantlyheavierin modelgroup , compared with
controlgroup.Celecoxibcangraduallyreducemyocardialhypertrophy.②TNF-αlevelsinplasma
werenosignificantdifferencesbetween2weeksand4weeksgroups ( P >0.05 ) .Inthemyocardial
tissue , thecontentofTNF-αin model2weeksgroupweresignificantlyincreased ( P <0.05 ) .
CelecoxibcanreducethethecontentofTNF-αlevels ( P <0.05 ) .At4weeks , thedifferences werenotstatisticallysignificant ( P >0.05 ) .③Comparedwiththecontrolgroup , theapoptosis
rateofmyocardialcellsin modelgroupandcelecoxibgroupweresignificantlyincreased ( P <
0.05 ), andcelecoxibtreatmentcansignificantlydecreasetheapoptosisofmyocardialhypertrophy
inrats ( P <0.05 ) .Conclusion Celecoxibinthetreatmentofmyocardialhypertrophyinratsmay
berelatedtotheTNF-αandapoptosisofmyocardialcells.

Key words: cardiachypertrophy , celecoxib , tumornecrosisfactor-alpha