Department of Cardiology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, People's Republic of China.
Department of Cardiology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, People's Republic of China; Department of Cardiology, Shanghai Putuo Central School of Clinical Medicine, Anhui Medical University, Shanghai 200062, People's Republic of China.
Phytomedicine. 2023 May;113:154681. doi: 10.1016/j.phymed.2023.154681. Epub 2023 Jan 30.
Ginsenoside Re is an active component in ginseng that confers protection against myocardial ischemia/reperfusion (I/R) injury. Ferroptosis is a type of regulated cell death found in various diseases.
Our study aims to investigate the role of ferroptosis and the protective mechanism of Ginsenoside Re in myocardial ischemia/reperfusion.
In the present study, we treated rats for five days with Ginsenoside Re, then established the myocardial ischemia/reperfusion injury rat model to detect molecular implications in myocardial ischemia/reperfusion regulation and to determine the underlying mechanism.
This study identifies the mechanism behind ginsenoside Re's effect on myocardial ischemia/reperfusion injury and its regulation of ferroptosis through miR-144-3p. Ginsenoside Re significantly reduced cardiac damage caused by ferroptosis during myocardial ischemia/reperfusion injury and glutathione decline. To determine how Ginsenoside Re regulated ferroptosis, we isolated exosomes from VEGFR2 endothelial progenitor cells after ischemia/reperfusion injury and performed miRNA profiling to screen the miRNAs aberrantly expressed in the process of myocardial ischemia/reperfusion injury and ginsenoside Re treatment. We identified that miR-144-3p was upregulated in myocardial ischemia/reperfusion injury by luciferase report and qRT-PCR. We further confirmed that the solute carrier family 7 member 11 (SLC7A11) was the target gene of miR-144-3p by database analysis and western blot. In comparison with ferropstatin-1, a ferroptosis inhibitor, in vivo studies confirmed that ferropstatin-1 also diminished myocardial ischemia/reperfusion injury induced cardiac function damage.
We demonstrated that ginsenoside Re attenuates myocardial ischemia/reperfusion induced ferroptosis via miR-144-3p/SLC7A11.
人参皂苷 Re 是人参中的一种活性成分，可提供针对心肌缺血/再灌注（I/R）损伤的保护。铁死亡是在各种疾病中发现的一种受调控的细胞死亡类型。
本研究旨在探究铁死亡在心肌缺血/再灌注中的作用以及人参皂苷 Re 的保护机制。
在本研究中，我们用人参皂苷 Re 处理大鼠 5 天，然后建立心肌缺血/再灌注损伤大鼠模型，以检测分子在心肌缺血/再灌注调节中的意义，并确定潜在的机制。
本研究通过 miR-144-3p 确定了人参皂苷 Re 对心肌缺血/再灌注损伤的作用及其对铁死亡的调节机制。人参皂苷 Re 显著减少了心肌缺血/再灌注损伤过程中铁死亡引起的心脏损伤和谷胱甘肽的下降。为了确定人参皂苷 Re 如何调节铁死亡，我们从缺血/再灌注损伤后的血管内皮祖细胞中分离出外泌体，并进行 miRNA 谱分析，以筛选在心肌缺血/再灌注损伤和人参皂苷 Re 治疗过程中异常表达的 miRNA。我们发现 miR-144-3p 在心肌缺血/再灌注损伤中上调，通过荧光素酶报告和 qRT-PCR 验证。我们进一步通过数据库分析和 Western blot 证实溶质载体家族 7 成员 11（SLC7A11）是 miR-144-3p 的靶基因。与铁死亡抑制剂 ferropstatin-1 相比，体内研究证实 ferropstatin-1 也可减轻心肌缺血/再灌注损伤引起的心脏功能损伤。
我们证实人参皂苷 Re 通过 miR-144-3p/SLC7A11 减轻心肌缺血/再灌注诱导的铁死亡。
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