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作 者:张金祝 李海德 尹桂华 姚宗芹 宋杰 赵蒙 赵明明 ZHANG Jinzhu;LI Haide;YIN Guihua;YAO Zongqin;SONG Jie;ZHAO Meng;ZHAO Mingming(Linyi Central Hospital,Linyi 276400,China)
出 处:《山东医药》2021年第1期57-60,共4页Shandong Medical Journal
摘 要:目的探讨miRNA208a对扩张型心肌病模型大鼠心肌纤维化的影响。方法取30只成年Wistar大鼠,采用连续腹腔注射阿霉素法制备扩张型心肌病模型,按照随机数字表法将其随机分为mut-miRNA208a组、an⁃tagomiRNA208a组、pre-miRNA208a组,每组10只。分别转染含突变miRNA208a、抑制miRNA208a表达、过表达miR⁃NA208a的腺相关病毒质粒。转染成功72 h后,应用动物心脏彩超检测各组大鼠心功能相关指标:心室舒张末期内径(LVEDD)、心室收缩末期内径(LVESD)、左心室射血分数(LVEF)。计算心脏指数(HWI);检测各组大鼠心肌组织中内皮素(ET)、β心肌肌球蛋白重链(MHC-β)、胶原蛋白Ⅰ(COL-Ⅰ)的表达水平。结果三组大鼠HWI、LVEDD、LVESD、LVEF,ET、MHC-β、COL-ⅠRNA及蛋白表达比较,差异均有统计学意义(P均<0.05)。与mut-miRNA208a组、pre-miRNA208a组相比,antagomiRNA208a组大鼠心功能好转,心肌组织中ET、βMHC、COL-Ⅰ表达下调,心肌间质纤维化程度明显减轻。结论miRNA208a可通过作用于其靶标ET、MHC-β促进COL-Ⅰ高表达在扩张型心肌病心肌纤维化的发生发展过程中起到重要作用。Objective To investigate the effect of miRNA208a on myocardial fibrosis in rats with dilated cardiomy⁃opathy.Methods We used doxorubicin to make 30 adult Wistar rats into dilated cardiomyopathy model rats,and then randomly divided them into the mut-miRNA208a group,antagomiRNA208a group,and pre-miRNA208a group,with 10 rats in each,which were transfected with the adeno-associated virus plasmids containing mutant miRNA208a,miR⁃NA208a inhibition,and miRNA208a overexpression,respectively.At 72 h after the successful transfection,animal heart color Doppler ultrasound was used to detect the relevant indicators of the heart function of rats in each group:ventricular end diastolic diameter(LVEDD),ventricular end-systolic diameter(LVESD),and left ventricular ejection fraction(LVEF);we calculated the heart index(HWI),and detected the expression levels of endothelin(ET),βcardiac myosin heavy chain(MHC-β),and collagen I(COL-I)in the myocardial tissues of rats in each group.Results Statistically sig⁃nificant differences were found in the expression levels of HWI,LVEDD,LVESD,LVEF,ET,MHC-β,COL-I RNA and protein between the three groups(all P<0.05).Compared with the mut-miRNA208a group and pre-miRNA208a group,the cardiac function of rats in the antagomiRNA208a group improved,the expression of ET,MHC-βand COL-1 in the myo⁃cardial tissues was down-regulated,and the myocardial interstitial fibrosis was significantly alleviated.Conclusion MiRNA208a can promote the high expression of COL-1 by acting on its targets ET and MHC-β,which plays an important role in the development and progression of myocardial fibrosis in dilated cardiomyopathy.
关 键 词:扩张型心肌病 miRNA208a 内皮素 β心肌肌球蛋白重链 胶原蛋白Ⅰ 心肌纤维化
分 类 号:R542.2[医药卫生—心血管疾病]
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