Proteasome inhibitor MG-132 improves myocadial hypertrophy after myocardial infarction in rats

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.12 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 were designated as sham-operated group(SH)group.Rats in MG group were treated with MG-132(0.1 mg/kg,daily)through intraperitoneal injection for 28 days,rats in MI group and SH group were given normal saline as control.On 28th day,left ventricle posterior wall thickness was measured by echocardiography and the left weight index was 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(P0.01).The values of myocardial cell direct,perimeter and surface area in non-infarct area were significantly increased in MI group and MG group(P0.01).However,the values of above makers in MG group were notably decreased as compared with those in MI group(P0.01).Moreover,the mRNA and protein levels of NF-kappaB P65 and IL-1βin MG group were lower than those in MI group(P0.01).Conclusions Myocadial hypertrophy following acute myocardial infarction is improved by MG-132 through suppressing NF-kappaB activation and the expression of inflammatory factor such as IL-1β in rats.