%0 Journal Article
%T 上调Cdr1as表达对急性心肌梗死大鼠心肌细胞凋亡的影响<br>Effect of upregulating Cdr1as expression on cardiomyocyte apoptosis in rats with acute myocardial infarction
%A 张
%A 杰
%A 贾丽萍
%A 周
%A 辉
%A 刘
%A 亮
%A 银鹏飞
%A 陈文强
%A 苏
%A 兴
%J 郑州大学学报（医学版）
%D 2018
%R 10.13705/j.issn.1671-6825.2018.04.004
%X 目的:探讨上调小脑变性相关蛋白1的反义转录物(Cdr1as)表达对急性心肌梗死(AMI)大鼠心肌细胞凋亡的影响。方法:将40只SD大鼠随机分为假手术组、模型组、空载体组和Cdr1as组,每组10只。模型组、空载体组和Cdr1as组采用冠状动脉左前降支结扎法建立AMI大鼠模型; 术前12 h分别心肌内注射生理盐水、pcDNA和pcDNA-Cdr1as溶液。术后1周,心脏彩超检测大鼠心脏功能; 然后取心肌组织,TTC染色法检测心肌梗死面积,TUNEL法检测心肌细胞凋亡指数,比色法检测Caspase-3活性,qRT-PCR检测Cdr1as表达水平,Western blot法检测Bcl-2和Bax蛋白。结果:与假手术组相比,模型组、空载体组和Cdr1as组心肌组织中Cdr1as表达水平、心肌细胞凋亡指数、Caspase-3活性、Bax蛋白表达水平以及左室长轴缩短分数、左室射血分数均升高,而左室收缩末期内径、左室舒张末期内径、心肌组织中Bcl-2蛋白表达水平均降低(P<0.05); Cdr1as组上述指标变化更显著(P<0.05)。Cdr1as组心肌梗死面积大于模型组和空载体组(P<0.05)。结论:Cdr1as可能通过间接调控Caspase-3、Bcl-2和Bax的表达,诱导心肌细胞凋亡,促进心肌梗死。<br>Aim:To investigate the effect of upregulating the expression of Cdr1as on cardiomyocyte apoptosis in rats with acute myocardial infarction(AMI).Methods:A total of 40 SD rats were randomly allocated into sham operation group, model group, empty vector group and Cdr1as group.The rats in the model group, empty vector group and Cdr1as group were ligated the left anterior descending branch of the coronary artery to establish the AMI models, and were intramyocardially injected with normal saline, pcDNA and pcDNA-Cdr1as solution before the operation.One week after the operation, cardiac function of rats was detected by color Doppler ultrasound, infarct size was detected by TTC staining, myocardial apoptosis index was detected by TUNEL, Caspase-3 activity in myocardium was detected by colorimetric method, the expression of Cdr1as in myocardial tissue was detected by qRT-PCR, and the expressions of Bcl-2 and Bax protein in myocardium was detected by Western blot.Results:Compared with those of the sham operation group, the expression level of Cdr1as, left ventricular fractional shortening, left ventricular ejection fraction, myocardial apoptosis index, Caspase-3 activity and Bax protein expression were increased, while left ventricular end systolic diameter, left ventricular end diastolic diameter and Bcl-2 protein expression were decreased in the model group, empty vector group and Cdr1as group(P<0.05), and the amplitude of variation of each index in the Cdr1as group was higher than the model group and empty vector group(P<0.05). The myocardial infarct size of the Cdr1as group was larger than those of the model group and empty vector group(P<0.05).Conclusion:Cdr1as could induce cardiomyocyte apoptosis and aggravate myocardial infarction by regulating the expressions of Caspase-3,Bax and Bcl-2
%K Cdr1as
%K 急性心肌梗死
%K 细胞凋亡
%K Caspase-3
%K Bcl-2
%K Bax&lt
%K br&gt
%K Cdr1as
%K acute myocardial infarction
%K apoptosis
%K Caspase-3
%K Bcl-2
%K Bax
%U http://jms.zzu.edu.cn/oa/darticle.aspx?type=view&id=201806018