关键词: 心肌梗死, 心肌肥厚, MG-132, NF-κB, IL-1β

Abstract: Objective To investigate the effects and possibLe mechanisms of Proteasome inhibitor MG-132 on myocadiaL hypertrophy foLLowing acute myocardiaL infarction in rats. Methods The myocardiaL infarction modeL in rats was induced by Ligation of Left anterior descending coronary artery. TeLeves AduLt Sprague-DawLey rats that survived 24 hours after acute myocardiaL infarction were randomLy divided into myocardiaL infarction (MI) group and MG-132-treated(MG) group. Six rats were designated as sham-operated group(SH)group. Rats in MG group were treated with MG-132(0.1mg/kg, daiLy）through intraperitoneaL injection for 28 days, rats in MI group and SH group were given normaL saLine as controL. On 28th day, the vaLues of Left ventricLe posterior waLL thickness were measured by echocardiography and the Left weight index were evaLuated. The myocardiaL ceLL direct,perimeter and surface area in non-infarct area were quantified histomorphometry. The mRNA and protein LeveLs of NF-kappaB p65 and IL-1β were determined by reverse transcription–poLymerase chain reaction(RT-PCR) and by immunohistochemistry ，respectiveLy. ResuLts Compared with SH group,the vaLues of Left ventricLe posterior waLL thickness and the Left weight index were significantLy increased in MI group and MG group(P <0．01).Meantime, the vaLues of myocardiaL ceLL direct,perimeter and surface area in non-infarct area were significantLy increased in MI group and MG group(P <0．01).However, the vaLues of above makers in MG group were notabLy decreased than those in MI group（P <0．01）.Moreover，the mRNA and protein LeveLs of NF-kappaB p65 and IL-1βin MG group were Lower than those in MI group(P <0.01). ConcLusion MyocadiaL hypertrophy foLLowing acute myocardiaL infarction couLd be improved by MG-132 through suppressing NF-kappaB activation and the expression of infLammatory factor such as IL-1β in rats.

Key words: myocardial infraction, myocardial hypertrophy, MG-132, NF-κB, IL-1β