首页> 外文期刊>European review for medical and pharmacological sciences. >MiR-808 inhibits cardiomyocyte apoptosis and expressions of caspase-3 and caspase-9 in rats with myocardial infarction by regulating TGF-β1 signaling pathway
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MiR-808 inhibits cardiomyocyte apoptosis and expressions of caspase-3 and caspase-9 in rats with myocardial infarction by regulating TGF-β1 signaling pathway

机译:MiR-808通过调节TGF-β1信号通路,在大鼠中抑制心肌细胞凋亡和Caspase-3和Caspase-9的表达

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OBJECTIVE: To investigate the effects of micro ribonucleic acid (miR)-808 on cardiomyocyte apoptosis and expressions of caspase-3 and caspase-9 in rats with myocardial infarction (MI) by regulating the transforming growth factor-β1 (TGF-β1) signaling pathway. MATERIALS AND METHODS: A total of 24 specific pathogen-free female Sprague-Dawley rats were enrolled and randomly divided into normal group, model group, and miR-808 group, 8 rats in each group. In the model group and miR-808 group, MI model was prepared by ligation of the left anterior descending coronary artery in the rats. The miR-808 group was transfected with miR-808 lentivirus after the model was established. After one week of intervention, the expression of TGF-β1 was detected by reverse transcription-polymerase chain reaction (RT-PCR). The cardiac function of rats was determined by echocardiography. The myocardium of rats was observed by Masson staining. The cardiomyocyte apoptosis of rats was examined by TdT-mediated dUTP-biotin nick end labeling (TUNEL) method. The expression levels of caspase-3 and caspase-9 were detected by Western blotting. RESULTS: The expression of TGF-β1 mRNA was higher in the model group than that in the normal group (p0.05), but compared with that in the model group, it was lower in the miR-808 group. The myocardial function and cardiomyocyte survival rate in the miR-808 group was better and higher than those in the model group (p0.05). The expression levels of caspase-3 and caspase-9 in the miR-808 group were lower than those in the model group (p0.05). CONCLUSIONS: MiR-808 can inhibit cardiomyocyte apoptosis in rats with MI by down-regulating TGF-β1 expression and inhibiting the expressions of caspase-3 and caspase-9.
机译:目的:通过调节转化生长因子-β1(TGF-β1)信号传导,探讨微核糖核酸(MIR)-808对心肌梗死(MI)的大鼠心肌细胞凋亡和Caspase-3和Caspase-9表达的影响途径。材料和方法:共进行24种特异性病原体的雌性Sprague-Dawley大鼠并随机分为每组的正常组,模型组和MiR-808组,8只大鼠。在模型组和miR-808组中,通过结扎大鼠左前期下降冠状动脉来制备MI模型。在建立模型后,用miR-808慢病毒​​转染miR-808组。干预一周后,通过逆转录聚合酶链反应(RT-PCR)检测TGF-β1的表达。大鼠的心脏功能由超声心动图测定。大鼠染色观察大鼠的心肌。通过TDT介导的DUTP-BIOTIN切口末端标记(TUNEL)方法检查大鼠的心肌细胞凋亡。通过蛋白质印迹检测Caspase-3和Caspase-9的表达水平。结果:模型组的TGF-β1mRNA的表达比正常组在模型组(P <0.05)中,但与模型组中的比较,MiR-808组中较低。 MiR-808组中的心肌功能和心肌细胞存活率更好,高于模型组中的生存率(P <0.05)。 miR-808组中Caspase-3和Caspase-9的表达水平低于模型组中的Caspase-9(P <0.05)。结论:MIR-808通过抑制TGF-β1表达和抑制Caspase-3和Caspase-9的表达,MiR-808可以抑制MI大鼠的心肌细胞凋亡。

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