活性氧在心肌缺血再灌注过程中对心脏是造成损伤还是起到保护作用？基于实验和临床数据的分析

Do reactive oxygen species damage or protect the heart in ischemia and reperfusion? Analysis on experimental and clinical data.

作者信息

Maslov Leonid N, Naryzhnaya Natalia V, Sirotina Maria, Mukhomedzyanov Alexandr V, Kurbatov Boris K, Boshchenko Alla A, Ma Huijie, Zhang Yi, Fu Feng, Pei Jianming, Azev Viacheslav N, Pereverzev Vladimir A

机构信息

Cardiology Research Institute, Tomsk National Research Medical Center, the Russian Academy of Sciences, Tomsk, Tomsk Region 634012, Russia.

Department of Physiology, Hebei Medical University, Shijiazhuang, Hebei 050017, China.

出版信息

J Biomed Res. 2023 Jul 28;37(4):268-280. doi: 10.7555/JBR.36.20220261.

DOI:10.7555/JBR.36.20220261

PMID:37503710

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10387750/

Abstract

The role of reactive oxygen species (ROS) in ischemic and reperfusion (I/R) injury of the heart has been discussed for more than 40 years. It has been demonstrated that reperfusion triggers a multiple increase in free radical generation in the isolated heart. Antioxidants were found to have the ability to mitigate I/R injury of the heart. However, it is unclear whether their cardioprotective effect truly depends on the decrease of ROS levels in myocardial tissues. Since high doses and high concentrations of antioxidants were experimentally used, it is highly likely that the cardioprotective effect of antioxidants depends on their interaction not only with free radicals but also with other molecules. It has been demonstrated that the antioxidant N-2-mercaptopropionyl glycine or NDPH oxidase knockout abolished the cardioprotective effect of ischemic preconditioning. Consequently, there is evidence that ROS protect the heart against the I/R injury.

摘要

活性氧（ROS）在心脏缺血再灌注（I/R）损伤中的作用已被讨论了40多年。研究表明，再灌注会引发离体心脏自由基生成的多重增加。人们发现抗氧化剂具有减轻心脏I/R损伤的能力。然而，目前尚不清楚它们的心脏保护作用是否真的取决于心肌组织中ROS水平的降低。由于实验中使用了高剂量和高浓度的抗氧化剂，因此抗氧化剂的心脏保护作用很可能不仅取决于它们与自由基的相互作用，还取决于它们与其他分子的相互作用。已经证明，抗氧化剂N-2-巯基丙酰甘氨酸或NDPH氧化酶基因敲除会消除缺血预处理的心脏保护作用。因此，有证据表明ROS可保护心脏免受I/R损伤。