首页> 美国卫生研究院文献>Oxidative Medicine and Cellular Longevity >Amifostine Pretreatment Attenuates Myocardial Ischemia/Reperfusion Injury by Inhibiting Apoptosis and Oxidative Stress
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Amifostine Pretreatment Attenuates Myocardial Ischemia/Reperfusion Injury by Inhibiting Apoptosis and Oxidative Stress

机译:氨磷汀预处理可通过抑制细胞凋亡和氧化应激减轻心肌缺血/再灌注损伤。

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摘要

The present study was aimed at investigating the effect of amifostine on myocardial ischemia/reperfusion (I/R) injury of mice and H9c2 cells cultured with TBHP (tert-butyl hydroperoxide). The results showed that pretreatment with amifostine significantly attenuated cell apoptosis and death, accompanied by decreased reactive oxygen species (ROS) production and lower mitochondrial potential (ΔΨm). In vivo, amifostine pretreatment alleviated I/R injury and decreased myocardial apoptosis and infarct area, which was paralleled by increased superoxide dismutase (SOD) and reduced malondialdehyde (MDA) in myocardial tissues, increased Bcl2 expression, decreased Bax expression, lower cleaved caspase-3 level, fewer TUNEL positive cells, and fewer DHE-positive cells in heart. Our results indicate that amifostine pretreatment has a protective effect against myocardial I/R injury via scavenging ROS.
机译:本研究旨在调查氨磷汀对小鼠和心肌中TBHP(叔丁基过氧化氢)培养的H9c2细胞的心肌缺血/再灌注(I / R)损伤的作用。结果表明,氨磷汀预处理可显着降低细胞凋亡和死亡,同时减少活性氧(ROS)的产生和降低线粒体电位(ΔΨm)。在体内,氨磷汀预处理可减轻I / R损伤并减少心肌细胞凋亡和梗塞面积,这与心肌组织中超氧化物歧化酶(SOD)升高和丙二醛(MDA)降低,Bcl2表达增加,Bax表达降低,半胱天冬酶裂解降低有关3级,心脏中的TUNEL阳性细胞更少,而DHE阳性细胞更少。我们的结果表明,氨磷汀预处理通过清除ROS对心肌I / R损伤具有保护作用。

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