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MiR-181a affects myocardial ischemia-reperfusion injury in rats via regulating akt signaling pathway

L-X Zhang1, F Ding, C-Q Wang

  • 1Department of Gerontology, The Third Hospital of Hebei Medical University, Shijiazhuang, China. daylight1981@126.com.

European Review for Medical and Pharmacological Sciences
|August 1, 2019
PubMed
Abstract

Insights

Micro ribonucleic acid (miR)-181a activation of the Akt pathway inhibits myocardial cell apoptosis, significantly alleviating myocardial ischemia-reperfusion injury (MIRI) in rats.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Myocardial ischemia-reperfusion injury (MIRI) is a critical clinical issue.
  • Understanding the molecular mechanisms underlying MIRI is essential for developing effective treatments.

Purpose of the Study:

  • To investigate the role of micro ribonucleic acid (miR)-181a in MIRI.
  • To explore the regulatory effect of miR-181a on the protein kinase B (Akt) signaling pathway in MIRI.

Main Methods:

  • A rat model of MIRI was established.
  • Rats were divided into sham, ischemia-reperfusion (I/R), and miR-181a treatment groups.
  • Cardiac function, apoptosis, nitric oxide (NO) levels, and protein expression (Akt, eNOS, Caspase-3, TNF-α) were assessed.

Main Results:

  • I/R significantly impaired cardiac function and increased myocardial apoptosis.
  • miR-181a treatment attenuated I/R-induced cardiac dysfunction and apoptosis.
  • miR-181a upregulated Akt and endothelial NO synthase (eNOS) phosphorylation and NO levels, while decreasing Caspase-3 and TNF-α expression.

Conclusions:

  • miR-181a plays a protective role in MIRI.
  • miR-181a activates the Akt/eNOS pathway, inhibiting myocardial cell apoptosis.
  • Targeting miR-181a may be a therapeutic strategy for MIRI.

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