Piceatannol protects against myocardial ischemia/reperfusion injury by inhibiting ferroptosis via Nrf-2 signaling-mediated iron metabolism

心肌缺血 苦参素 再灌注损伤 缺血 化学 细胞损伤 药理学 细胞损伤 细胞凋亡 抗氧化剂 细胞 程序性细胞死亡 氧化应激 医学 生物化学 心脏病学 内科学 白藜芦醇
作者
Mengmei Zhu,Tianhao Zhao,Binshan Zha,Guiyang Zhang,Weiwei Qian,Xinya Wang,Qiuju Zhao,Shuo Chen,Ze-ping Hu,Liuyi Dong
出处
期刊:Biochemical and Biophysical Research Communications [Elsevier]
卷期号:700: 149598-149598 被引量:3
标识
DOI:10.1016/j.bbrc.2024.149598
摘要

Myocardial tissue ischemia damages myocardial cells. Although reperfusion is an effective technique to rescue myocardial cell damage, it may also exacerbate myocardial cell damage. Ferroptosis, an iron-dependent cell death, occurs following myocardial ischemia-reperfusion (I/R). Piceatannol (PCT) is a natural stilbene compound with excellent antioxidant properties that protect against I/R injury and exerts protective effects against ferroptosis-induced cardiomyocytes following I/R injury; however, the exact mechanism remains to be elucidated. This study aims to investigate the protective effect and mechanism of PCT on myocardial ischemia-reperfusion injury. An ischemia-reperfusion model was established via ligation of the left anterior descending branch of mice's hearts and hypoxia-reoxygenation (H/R) of cardiomyocytes. During ischemia-reperfusion, Nuclear factor E2-related factor 2 (Nrf-2) expression was downregulated, the left ventricular function was impaired, intracellular iron and lipid peroxidation product levels were elevated, and cardiomyocytes underwent ferroptosis. Furthermore, ferroptosis was enhanced following treatment with an Nrf-2 inhibitor. After PCT treatment, Nrf-2 expression significantly increased, intracellular ferrous ions and lipid peroxidation products significantly reduced, Ferroportin1 (FPN1) expression increased, and transferrin receptor-1 (TfR-1) expression was inhibited. PCT regulates iron metabolism through Nrf-2 to protect against myocardial cell ferroptosis induced by myocardial I/R injury.
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