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氨磷汀预处理通过抑制细胞凋亡和氧化应激减轻心肌缺血/再灌注损伤。

Amifostine Pretreatment Attenuates Myocardial Ischemia/Reperfusion Injury by Inhibiting Apoptosis and Oxidative Stress.

作者信息

Wu Shao-Ze, Tao Lu-Yuan, Wang Jiao-Ni, Xu Zhi-Qiang, Wang Jie, Xue Yang-Jing, Huang Kai-Yu, Lin Jia-Feng, Li Lei, Ji Kang-Ting

机构信息

Department of Cardiology, The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou 325000, China.

出版信息

Oxid Med Cell Longev. 2017;2017:4130824. doi: 10.1155/2017/4130824. Epub 2017 Mar 14.

DOI:10.1155/2017/4130824
PMID:28392886
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5368387/
Abstract

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.

摘要

本研究旨在探讨氨磷汀对小鼠心肌缺血/再灌注（I/R）损伤以及用叔丁基过氧化氢（TBHP）培养的H9c2细胞的影响。结果表明，氨磷汀预处理可显著减轻细胞凋亡和死亡，同时活性氧（ROS）生成减少，线粒体膜电位（ΔΨm）降低。在体内，氨磷汀预处理减轻了I/R损伤，减少了心肌细胞凋亡和梗死面积，同时心肌组织中超氧化物歧化酶（SOD）增加、丙二醛（MDA）减少，Bcl2表达增加、Bax表达减少，裂解的半胱天冬酶-3水平降低，TUNEL阳性细胞减少，心脏中DHE阳性细胞减少。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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5908/5368387/8c49a1c2cc57/OMCL2017-4130824.009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5908/5368387/5b016dbb92f3/OMCL2017-4130824.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5908/5368387/c2ca9981c69d/OMCL2017-4130824.006.jpg
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