【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。更多还原

【Abstract】 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.更多还原