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首页> 美国卫生研究院文献>Antioxidants >Assessing the Efficacy of Dietary Selenomethionine Supplementation in the Setting of Cardiac Ischemia/Reperfusion Injury
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Assessing the Efficacy of Dietary Selenomethionine Supplementation in the Setting of Cardiac Ischemia/Reperfusion Injury

机译：评估饮食中补充硒代蛋氨酸在心脏缺血/再灌注损伤中的功效

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摘要

Oxidative stress is a major hallmark of cardiac ischemia/reperfusion (I/R) injury. This partly arises from the presence of activated phagocytes releasing myeloperoxidase (MPO) and its production of hypochlorous acid (HOCl). The dietary supplement selenomethionine (SeMet) has been shown to bolster endogenous antioxidant processes as well as readily react with MPO-derived oxidants. The aim of this study was to assess whether supplementation with SeMet could modulate the extent of cellular damage observed in an in vitro cardiac myocyte model exposed to (patho)-physiological levels of HOCl and an in vivo rat model of cardiac I/R injury. Exposure of the H9c2 cardiac myoblast cell line to HOCl resulted in a dose-dependent increase in necrotic cell death, which could be prevented by SeMet supplementation and was attributed to SeMet preventing the HOCl-induced loss of mitochondrial inner trans-membrane potential, and the associated cytosolic calcium accumulation. This protection was credited primarily to the direct oxidant scavenging ability of SeMet, with a minor contribution arising from the ability of SeMet to bolster cardiac myoblast glutathione peroxidase (GPx) activity. In vivo, a significant increase in selenium levels in the plasma and heart tissue were seen in male Wistar rats fed a diet supplemented with 2 mg kg SeMet compared to controls. However, SeMet-supplementation demonstrated only limited improvement in heart function and did not result in better heart remodelling following I/R injury. These data indicate that SeMet supplementation is of potential benefit within pathological settings where excessive HOCl is known to be generated but has limited efficacy as a therapeutic agent for the treatment of heart attack.
机译：氧化应激是心脏缺血/再灌注（I / R）损伤的主要标志。这部分是由于活化的吞噬细胞释放出髓过氧化物酶（MPO）及其产生的次氯酸（HOCl）引起的。膳食补充硒代蛋氨酸（SeMet）已显示出可增强内源性抗氧化剂过程，并易于与MPO衍生的氧化剂发生反应。这项研究的目的是评估补充SeMet是否可以调节在暴露于HOCl病理生理水平的体外心脏心肌细胞模型和心脏I / R损伤的体内大鼠模型中观察到的细胞损伤程度。 H9c2心肌成肌细胞系暴露于HOCl导致坏死细胞死亡的剂量依赖性增加，可以通过补充SeMet来预防，这归因于SeMet阻止了HOCl诱导的线粒体内部跨膜电位的丧失，并且相关的胞质钙积累。这种保护作用主要归功于SeMet的直接氧化剂清除能力，而SeMet增强心脏成肌细胞谷胱甘肽过氧化物酶（GPx）活性的能力仅占很小的比例。在体内，与对照相比，在饲喂补充了2 mg kg SeMet的日粮的雄性Wistar大鼠中，血浆和心脏组织中硒水平显着增加。但是，SeMet的补充仅显示了有限的心脏功能改善，并没有导致I / R损伤后更好的心脏重塑。这些数据表明，SeMet补充剂在病理环境中具有潜在的益处，在该环境中，已知会生成过量的HOCl，但作为治疗心脏病的治疗剂的功效有限。

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