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Expression of miR-223-3p in a rat model of myocardial infarction and the effects of miR-223-3p on cardiomyocytes
Frontiers in Life Science ( IF 1.333 ) Pub Date : 2020-08-07 , DOI: 10.1080/26895293.2020.1796827
Zhidong Zhang 1 , Gang Qiao 1 , Zhigang Sun 1 , Xiaosan Chen 1 , Jianyang Liu 1 , Wei Lu 1 , Gangqiang Zou 1
Affiliation  

ABSTRACT

This study aimed to investigate the expression of miR-223-3p in a rat model of myocardial infarction and the effects of miR-223-3p on cardiomyocytes. Forty rats were randomly divided into mock surgical, model (acute myocardial infarction (AMI) group (AMIG)), AMI + miR-223-3p adenovirus (intervention group (IG)), and AMI + scramble-NC (negative control group (NCG)) groups. Cardiac function was assessed by small animal echocardiography. Reverse transcription polymerase chain reaction was used to quantify the expression of miR-223-3p. The expression levels of miR-233-3p and SOX6 mRNA in the blank control group (BCG) and mock surgical group (MSG) were lower than those in the AMIG, IG, and NCG (P < 0.05), while the cardiac function indices of the BCG and MSG were higher than those of the AMIG, IG, and NCG (P < 0.05). The expression levels of miR-233-3p and SOX6 mRNA in the AMIG and NCG were significantly higher than those in the IG, while their cardiac function indices were significantly lower than those in the IG. Our findings indicate that the silencing of miR-223-3p effectively improves the cardiac function of rats, and the overexpression of miR-223-3p promotes the apoptosis of cardiomyocytes. Thus, miR-223-3p may be a new therapeutic target for AMI.



中文翻译:

miR-223-3p在大鼠心肌梗死模型中的表达及miR-223-3p对心肌细胞的影响

摘要

这项研究旨在调查miR-223-3p在大鼠心肌梗死模型中的表达以及miR-223-3p对心肌细胞的影响。40只大鼠随机分为模拟手术组,模型组(急性心肌梗死(AMI)组(AMIG)),AMI + miR-223-3p腺病毒(干预组(IG))和AMI + scramble-NC(阴性对照组( NCG))组。通过小动物超声心动图评估心脏功能。逆转录聚合酶链反应用于定量miR-223-3p的表达。空白对照组(BCG)和模拟手术组(MSG)的miR-233-3p和SOX6 mRNA的表达水平低于AMIG,IG和NCG(P  <0.05),而心功能指数BCG和MSG的百分比高于AMIG,IG和NCG的百分比(P  <0.05)。AMIG和NCG中miR-233-3p和SOX6 mRNA的表达水平明显高于IG,而其心脏功能指数明显低于IG。我们的发现表明,沉默miR-223-3p可以有效改善大鼠的心脏功能,而miR-223-3p的过表达可以促进心肌细胞的凋亡。因此,miR-223-3p可能是AMI的新治疗靶标。

更新日期:2020-08-08
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