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Protective effect of erythropoietin against myocardial injury in rats with sepsis and its underlying mechanisms

机译:促红细胞生成素对脓毒症大鼠心肌的保护作用及其潜在机制

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The aim of this study was to investigate the protective effect of erythropoietin (EPO) against acute myocardial injury and its underlying mechanisms. Mice (n=146) were randomly divided in a double-blind manner into four groups, sham, Rocephin, EPO and sepsis, and mortality was observed on the seventh day after cecal ligation and puncture. In addition, a total of 252 rats were randomly divided into three groups, sham, EPO and sepsis, and indicators of cardiac function, inflammatory mediators and serum creatine kinase levels were assessed. Mitochondrial membrane potential, cell apoptosis and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B) p65 expression levels were detected using flow cytometry. Following intervention with EPO, the mortality rate in mice with sepsis was significantly reduced and the cardiac function of septic rats was significantly improved. In addition, the levels of inflammatory mediators, serum creatine kinase and apoptosis and the myocardial mitochondrial membrane potential and expression of NF-kappa B p65 in cardiac tissue were all improved following EPO treatment, and the differences between the results for the sepsis and EPO groups were statistically significant (P<0.05). These findings suggest that EPO reduces the myocardial inflammatory response in septic rats, attenuates the reduction in mitochondrial membrane potential and inhibits myocardial cell apoptosis by reducing NF-kappa B p65 expression, and therefore exerts a protective effect in the myocardium.
机译:这项研究的目的是调查促红细胞生成素(EPO)对急性心肌损伤的保护作用及其潜在机制。将n = 146的小鼠以双盲方式随机分为假手术,罗汉芬,EPO和败血症四组,并在盲肠结扎和穿刺后第7天观察死亡率。此外,将总共252只大鼠随机分为假手术,EPO和败血症三组,并评估心脏功能,炎症介质和血清肌酸激酶水平的指标。流式细胞术检测线粒体膜电位,细胞凋亡和核因子κ轻链增强的激活的B细胞(NF-κB)p65表达水平。 EPO干预后,脓毒症小鼠的死亡率显着降低,脓毒症大鼠的心脏功能得到明显改善。此外,EPO治疗后,心脏组织中炎症介质,血清肌酸激酶和细胞凋亡的水平以及心肌线粒体膜电位和NF-κBp65的表达均得到改善,脓毒症和EPO组的结果之间存在差异具有统计学意义(P <0.05)。这些发现表明,EPO通过降低NF-κBp65的表达来降低败血性大鼠的心肌炎性反应,减弱线粒体膜电位的降低,并抑制心肌细胞的凋亡,从而在心肌中发挥保护作用。

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