二硫代氨基甲酸吡咯烷对大鼠心肌梗死后心肌细胞肥大的影响  

The effects of pyrrolidine dithiocarbamate on myocadial hypertrophy after myocardial infarction in rats

作　　者：何明[1] 陈章荣[2] 罗开良[3] 丁绍平 王红英[1] 

机构地区：[1]云南省曲靖市第一人民医院心内科,655000 [2]云南大理医学院附属医院心内科 [3]重庆医科大学第二附属医院心内科

出　　处：《心肺血管病杂志》2012年第6期740-743,共4页Journal of Cardiovascular and Pulmonary Diseases

摘　　要：目的:探讨二硫代氨基甲酸吡咯烷(PDTC)对大鼠心肌梗死后心肌细胞肥大的影响及机制。方法:制作大鼠心肌梗死模型,随机分为PDTC干预(PD)组和心肌梗死对照(MI)组,另设假手术(SH)组,每组大鼠6只。PD组于术后24h腹腔注射PDTC(80 mg.kg-1.d-1),MI组及SH组注射0.9%氯化钠液对照。连续给药28 d后处死动物,计算心肌细胞面积、周长、平均直径。RT-PCR和免疫组化分别检测核转录因子-κBp65(NF-κBp65)及白介素-1β(IL-1β)的mRNA和蛋白质表达量。结果:与SH组比较,PD组和MI组的心肌细胞的直径、周长和表面积明显增大,NF-κBp65和IL-1β的mRNA及蛋白质表达量明显增加,差异均有统计学意义(P<0.01)。与MI组比较,PD组的心肌细胞的直径、周长和表面积改变明显减轻,NF-κBp65和IL-1β的mRNA及蛋白质表达量明显降低,差异有统计学意义(P<0.01)。结论:PDTC能一定程度地改善大鼠心肌梗死后心肌细胞肥大,其机制可能与抑制NF-κB激活,下调炎性细胞因子如IL-1β表达有关。Objective：To investigate the effects and possible mechanisms of pyrrolidine dithiocarbamate（PDTC） 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 PDTC-treated（PD） group.Six rats were designated as sham-operated group（SH group）.Rats in PD group were treated with PDTC（80 mg/kg,daily） through intraperitoneal injection for 28 days,rats in MI group and SH group were given normal saline as control.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 myocardial cell direct,perimeter and surface area in non-infarct area were significantly increased in MI group and PD group（P〈0.01）.The values of myocardial cell direct,perimeter and surface area in non-infarct area in PD 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 PD group were lower than those in MI group（P〈0.01）.Conclusion：Myocadial hypertrophy following acute myocardial infarction could be improved by PDTC through suppressing NF-kappaB activation and the expression of inflammatory factor such as IL-1β in rats.

关 键 词：心肌梗死 二硫代氨基甲酸吡咯烷 核转录因子 心肌细胞肥大 白介素-1Β 

分 类 号：R54[医药卫生—心血管疾病]