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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Mitochondrial permeability transition pore plays a role in the cardioprotection of CB2 receptor against ischemia-reperfusion injury
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Mitochondrial permeability transition pore plays a role in the cardioprotection of CB2 receptor against ischemia-reperfusion injury

机译：线粒体通透性过渡孔在CB2受体抵抗缺血再灌注损伤的心脏保护中起作用

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摘要

The aim of this study was to investigate whether the mitochondrial permeability transition pore (MPTP) opening was involved in the protective effects of CB2 receptor against ischemia-reperfusion (I-R) injury. For this, isolated perfused rat hearts were subjected to 30 min global ischemia followed by 120 min reperfusion, and left ventricle function was recorded. At the end of reperfusion, the infarct size in the hearts was measured by staining with triphenyltetrazolium chloride. MPTP opening and the mitochondrial membrane potential (ΔΦm) were measured by flow cytometry. Western blot analysis of cytochrome c in the mitochondrion and cytosol, as well as ERK1/2 and p-ERK1/2 were performed. Administration of CB2 receptor agonist JWH133 before ischemia significantly improved the recovery of cardiac ventricular function during reperfusion, increased coronary flow, reduced infarct size, prevented the loss of ΔΦm and MPTP opening, reduced the release of cytochrome c from mitochondria, and increased levels of p-ERK1/2. These effects of JWH133 were abolished by pretreatment with CB2 receptor antagonist AM630, or ERK1/2 inhibitor PD98059. Furthermore, JWH133 reversed the MPTP opening induced by atractyloside. The protective effect of JWH133 on the heart against I-R injury may be through increased ERK1/2 phosphorylation, inhibiting MPTP opening.
机译：这项研究的目的是调查线粒体通透性转换孔（MPTP）的开放是否参与了CB2受体对缺血再灌注（I-R）损伤的保护作用。为此，将离体的灌流大鼠心脏进行30分钟的整体缺血，然后再进行120分钟的再灌注，并记录左心室功能。在再灌注结束时，通过用氯化三苯基四唑鎓染色来测量心脏中的梗塞大小。通过流式细胞术测量MPTP开放度和线粒体膜电位（ΔΦm）。对线粒体和细胞质中的细胞色素c以及ERK1 / 2和p-ERK1 / 2进行了蛋白质印迹分析。缺血前给予CB2受体激动剂JWH133可显着改善再灌注期间心室功能的恢复，增加冠状动脉血流量，减小梗塞面积，防止ΔΦm和MPTP开口的丢失，减少线粒体中细胞色素c的释放以及p的水平升高-ERK1 / 2。通过使用CB2受体拮抗剂AM630或ERK1 / 2抑制剂PD98059进行预处理，可以消除JWH133的这些作用。此外，JWH133逆转了由白术苷诱导的MPTP开放。 JWH133对心脏的抗I-R损伤的保护作用可能是通过增加ERK1 / 2磷酸化来抑制MPTP开放。

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