δ-阿片受体作为药物研发中增强心脏对再灌注耐受性的分子靶点
δ-Opioid Receptor as a Molecular Target for Increasing Cardiac Resistance to Reperfusion in Drug Development.
作者信息
Naryzhnaya Natalia V, Mukhomedzyanov Alexander V, Sirotina Maria, Maslov Leonid N, Kurbatov Boris K, Gorbunov Alexander S, Kilin Mikhail, Kan Artur, Krylatov Andrey V, Podoksenov Yuri K, Logvinov Sergey V
机构信息
Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Science, Tomsk 634021, Russia.
Department of Histology, Embryology and Cytology, Siberian State Medical University, Tomsk 634050, Russia.
出版信息
Biomedicines. 2023 Jul 3;11(7):1887. doi: 10.3390/biomedicines11071887.
An analysis of published data and the results of our own studies reveal that the activation of a peripheral δ-opioid receptor (δ-OR) increases the cardiac tolerance to reperfusion. It has been found that this δ-OR is localized in cardiomyocytes. Endogenous opioids are not involved in the regulation of cardiac resistance to reperfusion. The infarct-limiting effect of the δ-OR agonist deltorphin II depends on the activation of several protein kinases, including PKCδ, ERK1/2, PI3K, and PKG. Hypothetical end-effectors of the cardioprotective effect of deltorphin II are the sarcolemmal K channels and the MPT pore.
已发表数据的分析以及我们自身研究结果表明，外周δ-阿片受体（δ-OR）的激活可增强心脏对再灌注的耐受性。已发现该δ-OR定位于心肌细胞中。内源性阿片类物质不参与心脏对再灌注耐受性的调节。δ-OR激动剂二乙氨苯丙酮II的梗死限制作用取决于几种蛋白激酶的激活，包括PKCδ、ERK1/2、PI3K和PKG。二乙氨苯丙酮II心脏保护作用的假定终效应器是肌膜钾通道和线粒体通透性转换孔。
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