MicroRNA-383-5p Regulates Oxidative Stress in Mice with Acute Myocardial Infarction through the AMPK Signaling Pathway via PFKM

Figure 3

Upregulation of miR-383-5p suppresses PFKM. The myocardial tissues used for following detections were, respectively, treated with sham, AMI+PBS, AMI+miR-383-5p agomir, and AMI+miR-383-5p agomir NC. (a) miR-383-5p expression of myocardial tissue of mice by RT-qPCR. (b, c) Protein expression of PFKM in the myocardial tissue of mice by western blot analysis. (d) SOD1 and SOD2 expression by western blot. (e, f) The mRNA expression results of SOD1 and SOD2 in the three groups were determined by real-time PCR. vs. the sham group; ^# vs. the AMI+PBS group; the results of miR-383-5p expression, PFKM mRNA, and protein expressions were regarded as measurement data, presented by and analyzed by one-way ANOVA. There were 10 mice in each group, and the experiment was repeated 3 times; miR-383-5p: microRNA-383-5p; PFKM: phosphofructokinase muscle-type; AMI: acute myocardial infarction.

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