广西医科大学学报2025，Vol.42Issue(2)：233-240,8.DOI:10.16190/j.cnki.45-1211/r.2025.02.010
LncRNA MIAT/miR-384-5p在急性心肌梗死大鼠中的作用机制研究
Study on the action mechanism of lncRNA MIAT/miR-384-5p in rats with acute myocardial infarction
摘要
Abstract
Objective:To investigate the role and molecular mechanism of lncRNA MIAT inhibition in acute myocardial infarction(AMI)in rats.Methods:Sixty male Sprague-Dawley(SD)rats were randomly divided into sham,AMI,AMI+si-NC,AMI+si-MIAT,AMI+si-MIAT+miR-NC antagomir,and AMI+si-MIAT+miR-384-5p antagomir groups.The target plasmids were transfected into the myocardial tissue through in situ multi-point in-jections to silence the expression of lncRNA MIAT and miR-384-5p in rats.After 24 hours of transfection,the AMI model was established by performing ligation of the left anterior descending branch of the coronary artery of the heart for a duration of 24 hours.After completing the modeling,the changes of heart rate(HR),left ven-tricular systolic pressure(LVSP),left ventricular end-diastolic pressure(LVEDP)and the maximum rate of rise and fall of left ventricular pressure(±dP/dtmax)were gauged by biosignal acquisition system.The 2,3,5,triphenyl-2Htetrazolium chloride(TTC)staining was used to determine the infarct size and the pathological changes in car-diomyocytes were observed by hematoxylin-eosin(HE)staining.The level of serum cardiac troponin-Ⅰ(cTn-Ⅰ)was detected by enzyme-linked immunosorbent assay(ELISA).Transmission electron microscope(TEM)was used to observe the number of autophagosomes.Reverse transcription-quantitative polymerase chain reaction(RT-qPCR)was used to detect lncRNA MIAT and miR-384-5p gene expression,and western blotting was used to de-tect autophagy-associated proteins Beclin1,Cathepsin D and LC3 expression.Results:Compared with the sham group,the expression of lncRNA MIAT was increased in rats with AMI(P＜0.01).Compared with the AMI+si-NC group,the knockdown of lncRNA MIAT led to an upregulation of miR-384-5p expression,an increase in the levels of HR,LVSP and+dp/dtmax,and a decrease in the levels of LVEDP and-dp/dtmax.TTC and HE staining revealed a decreased myocardial infarct size in AMI rats and improved cardiomyocyte morphology.Additionally,serum cTn-I levels were significantly reduced,the number of autophagosomes was decreased,and the protein ex-pression levels of Beclin1,Cathepsin D,and LC3 were down-regulated(all P＜0.05).The above effects of ln-cRNA MIAT knockdown were significantly reversed when co-administered with the miR-384-5p antagomir(all P＜0.05).Conclusion:Inhibition of lncRNA MIAT can alleviate AMI in rats,which is related to upregulation of miR-384-5p expression and inhibition of autophagy.关键词
lncRNA MIAT/急性心肌梗死/miR-384-5p/自噬Key words
lncRNA MIAT/acute myocardial infarction/miR-384-5p/autophagy分类
医药卫生引用本文复制引用
李灿,陈卉彬,简洁..LncRNA MIAT/miR-384-5p在急性心肌梗死大鼠中的作用机制研究[J].广西医科大学学报,2025,42(2):233-240,8.基金项目
国家自然科学基金资助项目(No.81760726) （No.81760726）
广西硕士研究生创新项目资助(No.YCSW2024457) （No.YCSW2024457）
