Key result
Deltorphin II reduces reperfusion infarct size via peripheral δ2 opioid receptor activation and MPTP closing.
Why the study?
Opioid peptides are potential treatments for acute myocardial infarction and reperfusion injury, but the molecular mechanism of their infarct-limiting effect in reperfusion remains unexplored.
Does deltorphin II reduce infarct size in rats subjected to coronary artery occlusion and reperfusion?
Does deltorphin II reduce infarct size in rats subjected to coronary artery occlusion and reperfusion?
Deltorphin II exerts cardioprotective, infarct-reducing effects during reperfusion through specific intracellular signaling pathways including PKCδ, PI3-kinase, and ERK1/2-kinase.
Deltorphin II confers reperfusion cardioprotection in rats; leaves open translation to human MI therapy.
The search for novel drugs for the treatment of acute myocardial infarction and reperfusion injury of the heart is an urgent aim of modern pharmacology. Opioid peptides could be such potential drugs in this area. However, the molecular mechanism of the infarct-limiting effect of opioids in reperfusion remains unexplored. The objective of this research was to study the signaling mechanisms of the cardioprotective effect of deltorphin II in reperfusion. Rats were subjected to coronary artery occlusion (45 min) and reperfusion (2 h). The ratio of infarct size/area at risk was determined. This study indicated that the cardioprotective effect of deltorphin II in reperfusion is mediated via the activation of peripheral δ2 opioid receptor (OR), which is most likely localized in cardiomyocytes. We studied the role of guanylyl cyclase, protein kinase Cδ (PKCδ), phosphatidylinositol-3-kinase (PI3-kinase), extracellular signal-regulated kinase-1/2 (ERK1/2-kinase), ATP-sensitive K+-channels (KATP channels), mitochondrial permeability transition pore (MPTP), NO synthase (NOS), protein kinase A (PKA), Janus 2 kinase, AMP-activated protein kinase (AMPK), the large conductance calcium-activated potassium channel (BKCa-channel), reactive oxygen species (ROS) in the cardioprotective effect of deltorphin II. The infarct-reducing effect of deltorphin II appeared to be mediated via the activation of PKCδ, PI3-kinase, ERK1/2-kinase, sarcolemmal KATP channel opening, and MPTP closing.
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Попов et al. (2023) studied acute myocardial infarction and reperfusion injury. Deltorphin II was evaluated on ratio of infarct size/area at risk. Deltorphin II reduced infarct size during reperfusion via activation of peripheral δ2 opioid receptors, PKCδ, PI3-kinase, ERK1/2-kinase, sarcolemmal KATP channel opening, and MPTP closing.
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