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远程缺血预处理对急性心肌梗死大鼠模型的心脏保护作用。

The Cardioprotective Effects of Remote Ischemic Conditioning in a Rat Model of Acute Myocardial Infarction.

机构信息

Department of Pharmacology, College of Basic Medical Sciences, Tianjin Medical University, Tianjin, China (mainland).

Tianjin Medical University General Hospital, Tianjin, China (mainland).

出版信息

Med Sci Monit. 2019 Mar 8;25:1769-1779. doi: 10.12659/MSM.914916.

DOI:10.12659/MSM.914916
PMID:30848248
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6419535/
Abstract

BACKGROUND Cardiac remote ischemic conditioning (RIC) is a noninvasive cardioprotective method in ischemia-reperfusion injury and acute myocardial infarction (AMI). The aims of this study were to investigate the effects of RIC in a rat model of AMI. MATERIAL AND METHODS Adult male Sprague-Dawley rats included the AMI group that underwent ligation of the left anterior descending (LAD) coronary artery (n=24), the RIC group that consisted the AMI rat model treated with RIC once daily in the left hind limb until days 1, 7 and 14 (n=24), and the sham group (n=24). Myocardial infarct size was measured by routine histology with triphenyltetrazolium chloride (TTC) and Masson's trichrome histochemical staining for myocardial necrosis and fibrosis, respectively. Serum levels of Bcl-2, Bax, caspase-3, and inducible nitric oxide synthase (iNOS) were measured by enzyme-linked immunosorbent assay (ELISA). The apoptosis index was detected using the TUNEL assay. Spectrophotometry of the myocardium was used to identify mitochondrial complexes and myocardial ATP. RESULTS The RIC group showed improved cardiac hemodynamics, reduced the size of the myocardial infarction, upregulated expression of Bcl-2, and down-regulation of the levels of Bax, caspase-3, and iNOS, and reduced cardiac myocyte apoptosis and inhibited the opening of the mitochondrial permeability transition pore (MPTP). CONCLUSIONS In a rat model of AMI, RIC improved the hemodynamic index, reduce the levels of apoptosis and myocardial injury, and improved mitochondrial function.

摘要

背景

心脏远程缺血预处理(RIC)是缺血再灌注损伤和急性心肌梗死(AMI)的一种非侵入性心肌保护方法。本研究旨在探讨 RIC 在 AMI 大鼠模型中的作用。

材料和方法

成年雄性 Sprague-Dawley 大鼠包括 AMI 组,该组大鼠结扎左前降支(LAD)冠状动脉(n=24),RIC 组由 AMI 大鼠模型组成,每天在左后肢接受 RIC 治疗一次,直至第 1、7 和 14 天(n=24),以及假手术组(n=24)。通过三苯基四唑氯(TTC)常规组织学和 Masson 三色组织化学染色分别测量心肌梗死面积以检测心肌坏死和纤维化,用酶联免疫吸附测定(ELISA)测量血清中 Bcl-2、Bax、caspase-3 和诱导型一氧化氮合酶(iNOS)的水平。用 TUNEL 检测法检测细胞凋亡指数。用分光光度法测定心肌线粒体复合物和心肌 ATP。

结果

RIC 组显示出改善的心脏血液动力学,减小了心肌梗死的面积,上调了 Bcl-2 的表达,下调了 Bax、caspase-3 和 iNOS 的水平,减少了心肌细胞凋亡,并抑制了线粒体通透性转换孔(MPTP)的开放。

结论

在 AMI 大鼠模型中,RIC 改善了血液动力学指数,降低了细胞凋亡和心肌损伤水平,并改善了线粒体功能。

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