Key result
MiR-451 upregulation reduces myocardial infarct size and cell apoptosis in rat ischemia-reperfusion injury.
Why the study?
The regulatory mechanism of miR-451 on HMGB1 expression and its protective role in myocardial ischemia-reperfusion injury were not fully understood.
Does miR-451 up-regulation reduce ischemia-reperfusion injury and regulate HMGB1 expression in a rat model?
Does miR-451 up-regulation reduce ischemia-reperfusion injury and regulate HMGB1 expression in a rat model?
p-value: p=<0.05
In a rat model, up-regulation of miR-451 protects myocardial cells against ischemia-reperfusion injury, likely by down-regulating HMGB1 expression at the transcriptional level and reducing oxidative stress and apoptosis.
miR-451 up-regulation may attenuate rat ischemia-reperfusion injury; leaves open translation to human cardioprotection.
This work aimed to understand the underlying mechanism of micro-ribonucleic acid (MicroRNA) (miR)-451 in ischemia-reperfusion injury (IRI) and the influences of miR-451 on high mobility group box 1 protein (HMGB1) in myocardial cells, 30 specific pathogen-free (SPF) male rats were selected and randomly rolled into 5 groups, which were a sham operation control (Control), an ischemia-reperfusion (I/R), aI/R+Ad-GFP, amiR-451 up-regulation (I/R+Ad-miR-451), and a miR-451 down-regulation groups (I/R+Ad-asmiR-451). There were 6 cases in each group. Myocardial cell apoptosis, the contents of serum lactic acid dehydrogenase (LDH), creatine kinase (CK), and malondialdehyde (MDA), the activity of superoxide dismutase (SOD), and the expressions of miR-451 and HMGB1mRNA were detected. Relative to those in I/R and I/R+Ad-GFP groups, the expressions of CD3+, CD4+, and CD4+/ CD8+ in I/R+Ad-miR-451 group reduced (P<0.05). The expressions of serum LDH and CK decreased (P<0.05). In contrast, MDA content and SOD activity enhanced (P<0.05). HMGB1 and Cleaved-caspase3 declined (P<0.05). Besides, miR-451 improved while the expression of HMGB1mRNA significantly reduced (P<0.05). miR-451 can regulate the expressions of HMGB1mRNA and its protein at the transcriptional level. miR-451 up-regulation can inhibit HMGB1 expression, relieve IRI, and protect myocardial cells, which may be achieved by improving oxidative stress injury and inhibiting cell apoptosis.
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Qiu et al. (2023) studied Myocardial ischemia-reperfusion injury (n=30). Ad-miR-451 (miR-451 up-regulation) vs. Ischemia-reperfusion alone (PBS injection) and I/R+Ad-GFP (empty vector) was evaluated on Myocardial infarction area (p=<0.05). Up-regulation of miR-451 via Ad-miR-451 significantly reduced myocardial infarction area, myocardial cell apoptosis, and HMGB1 expression in a rat model of ischemia-reperfusion injury (P<0.05).
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