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一氧化氮合酶、MPT 孔和蛋白激酶 A 在阿片受体激动剂 Delta 啡 II 心脏保护作用中的作用。

The Role of NO Synthase, MPT pore, and Protein Kinase A in the Cardioprotective Effect of the Opioid Receptor Agonist Deltorphin II.

机构信息

Cardiology Research Institute, Tomsk National Research Medical Center, Russian Academy of Sciences, Tomsk, Russia.

Branch of M. M. Shemyakin and Yu. A. Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, Pushchino, Moscow region, Russia.

出版信息

Bull Exp Biol Med. 2023 Apr;174(6):745-748. doi: 10.1007/s10517-023-05784-4. Epub 2023 May 10.

Abstract

In male Wistar rats, coronary occlusion (45 min) and reperfusion (120 min) were modeled. Selective δ-opioid receptor agonist (deltorphin II, 0.12 mg/kg) was administered intravenously 5 min before reperfusion; NO synthase inhibitor (L-NAME, 10 mg/kg), MPT pore blocker (atractyloside, 5 mg/kg), and protein kinase A inhibitor (H-89, 10 μg/kg) were administered intravenously 10 min before reperfusion. Deltorphin II administered before reperfusion led to a 2-fold decrease in the infarct size. The infarct-limiting effect of deltorphin II was associated with blockade of MPT pore. Protein kinase A and NO synthase were not involved in the cardioprotective effect of deltorphin II.

摘要

在雄性 Wistar 大鼠中,建立了冠状动脉闭塞(45 分钟)和再灌注(120 分钟)模型。选择性 δ-阿片受体激动剂(deltorphin II,0.12mg/kg)在再灌注前 5 分钟静脉注射;一氧化氮合酶抑制剂(L-NAME,10mg/kg)、MPT 孔阻滞剂(远志糖苷,5mg/kg)和蛋白激酶 A 抑制剂(H-89,10μg/kg)在再灌注前 10 分钟静脉注射。再灌注前给予 deltorphin II 可使梗死面积减少 2 倍。deltorphin II 的梗死限制作用与 MPT 孔的阻断有关。蛋白激酶 A 和一氧化氮合酶不参与 deltorphin II 的心脏保护作用。

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