沉默miR-208a对急性心肌梗死大鼠心室重构的影响及机制研究  

Effects and mechanism of silencing miR 208a on ventricular remodeling in rats with acute myocardial infarction

作　　者：刘国星 杜见霞 刘秀红[1] 杜亚军[1] 但国梅 王浩[1] 董振松 LIU Guoxing;DU Jianxia;LIU Xiuhong(Department of Cardiology,The First People’s Hospital of Zaoyang City,Hubei,Zaoyang 441200,China)

机构地区：[1]湖北省枣阳市第一人民医院心内科,441200

出　　处：《河北医药》2022年第1期36-40,共5页Hebei Medical Journal

摘　　要：目的探究沉默miR-208a对急性心肌梗死大鼠的心室重构的影响及相关机制。方法选取40只SD健康雄性大鼠,10只为正常组,其余30只建立急性心肌梗死模型,并分为模型组、过表达miR-208a组、沉默miR-208a组,对4组大鼠分别进行干预。检测大鼠心功能[左心室舒张末期内径(LVEDd)、左心室舒张末期容积(LVEDV)、左心室收缩末期内径(LVESd)],观察4组大鼠心脏外观,心肌梗死面积、心肌细胞凋亡情况,检测4组大鼠miR-146a表达,Western blot法检测[B淋巴细胞瘤-2基因(Bcl-2)、半胱氨酸天冬氨酸蛋白酶3(Caspase-3)、转化生长因子-β1(TGF-β1)、果蝇MAD类似基因2(Smad2)、果蝇MAD类似基因3(Smad3)]相对表达量,免疫透射比浊法检测谷胱甘肽过氧化物酶(GSH-Px)、过氧化脂质(LPO)、丙二醛(MDA)水平。结果过表达miR-208a组大鼠miR-208a、Bcl-2、Caspase-3、TGF-β1、Smad2、Smad3表达高于模型组和正常组,与模型组、过表达miR-208a组比较,沉默miR-208a组大鼠miR-208a、Bcl-2、Caspase-3、TGF-β1、Smad2、Smad3表达较低(P<0.05)。过表达miR-208a组大鼠LVEDd、LVEDV、LVESd水平高于模型组和正常组(P<0.05),与模型组、过表达miR-208a组比较,沉默miR-208a组大鼠LVEDd、LVEDV、LVESd水平较低(P<0.05)。与模型组、过表达miR-208a组比较,沉默miR-208a组大鼠心肌梗死面积、心肌细胞凋亡指数较低(P<0.05)。与模型组、过表达miR-208a组比较,沉默miR-208a组大鼠GSH-Px水平较高,LPO、MDA水平较低(P<0.05)。结论沉默急性心肌梗死大鼠miR-208a表达,能够靶向调控Bcl-2、Caspase-3表达,抑制心肌细胞凋亡,改善大鼠心室重构,能够减轻心肌组织氧化应激损伤以及心肌纤维化,为急性心肌梗死的临床治疗提供一定的参考依据。Objective To investigate the effects of silencing miR 208a on ventricular remodeling in rats with acute myocardial infarction(AMI)and the related mechanisms.Methods A total of 40 SD healthy male rats were enrolled in the study,in which,10 rats were enrolled as control group,and the rats models with AMI were established in the other 30 rats,who were divided into model group,miR 208a over-expressing group group,silencing miR 208a group.The cardiac function indexes including left ventricular end diastolic diameter(LVEDd),left ventricular end diastolic volume(LVEDV),left ventricular end systole diameter(LVESd)were detected.The cardiac appearance,the area of myocardial infarction and the apoptosis of myocardial cells were observed.The expression levels of miR 146a were detected.And the relative expression levels of Bcl 2,caspase 3,TGFβ1,Smad2,Smad3 were detected by Western Blot.Moreover the levels of GSH Px,LPO and MDA were detected by immunity transmission turbidimetry.Results The expression levels of miR 208a,Bcl 2,Caspase-3,TGFβ1,Smad2,Smad3 in miR 208a over-expressing group were significantly higher than those in model group and control group.As compared with those in model group and miR 208a over-expressing group,the expression levels of miR 208a,Bcl 2,caspase 3,TGFβ1,Smad2,Smad3 in silencing miR 208a group were significantly decreased(P<0.05).The levels of LVEDd,LVEDV and LVESd in miR 208a over-expressing group were significantly higher than those in model group and control group(P<0.05).As compared with those in model group and miR 208a over-expressing group,the levels of LVEDd,LVEDV and LVESd in silencing miR 208a group were significantly decreased(P<0.05).A compared with those in model group and miR 208a over-expressing group,the infarct size of myocardial and the myocardial apoptosis in silencing miR 208a group were significantly decreased (P<0.05).As compared with those in model group and miR 208a over-expressing group,the GSH Px levels in silencing miR 208a group were significantly increased,and the lev

关 键 词：心肌梗死 急性 心室重构 氧化应激 心肌纤维化 细胞凋亡 

分 类 号：R542.22[医药卫生—心血管疾病]