Xu Lili, Zhou Jiedong, Lou Haifei, Gu Haodi, Xu Haixia, Zhong Zuoquan, Lin Hui, Jiang Chengjian
Medical Research Center, Shaoxing People's Hospital, Shaoxing, China.
School of Medicine, Shaoxing University, Shaoxing, Zhejiang, China.
Front Cardiovasc Med. 2025 May 23;12:1506388. doi: 10.3389/fcvm.2025.1506388. eCollection 2025.
Myocardial ischemia-reperfusion injury is a pathological phenomenon that occurs after coronary blood flow restoration and poses a threat to patients' lives. Its mechanisms are closely related to oxidative stress and mitochondrial dysfunction. Yellow Wine Polyphenolic Compounds, a dietary polyphenol with significant antioxidant effects, have been shown to offer protection in various cardiovascular diseases. However, their role in MIRI remains under-researched.
experiments, TTC staining was used to assess myocardial viability, and cardiac ultrasound was employed to measure left ventricular ejection function. Morphological staining and detection of myocardial injury markers were used to evaluate cardiac damage. Transmission electron microscopy was used to observe mitochondrial morphology in myocardial tissue, and ELISA was performed to evaluate the activity of mitochondrial complexes. Adeno-associated virus knockdown was utilized to verify the role of Nrf2. In experiments, confocal microscopy was used to scan mitochondrial morphology in cardiomyocytes and to observe the intracellular localization of the Nrf2 molecule.
TTC staining showed that MIRI significantly increased the infarct size in the left ventricle, whereas pre-treatment with YWPC (Yellow Wine Polyphenol Compound) significantly reduced the infarct area. Cardiac ultrasound demonstrated that YWPC intervention preserved left ventricular ejection fraction. Morphological staining and detection of myocardial injury markers revealed that MIRI caused tissue edema, increased myocardial apoptosis and damage, but YWPC pre-treatment alleviated these injuries. Transmission electron microscopy showed that YWPC reversed the excessive mitochondrial fission caused by MIRI. Immunofluorescence indicated that YWPC significantly promoted Nrf2 nuclear translocation and increased the expression of downstream antioxidant molecules.
YWPC pre-treatment can protect myocardial tissue by reducing the excessive mitochondrial fission induced by MIRI, and Nrf2 mediates these effects.
心肌缺血再灌注损伤是冠状动脉血流恢复后发生的一种病理现象，对患者生命构成威胁。其机制与氧化应激和线粒体功能障碍密切相关。黄酒多酚化合物是一种具有显著抗氧化作用的膳食多酚，已被证明在各种心血管疾病中具有保护作用。然而，它们在心肌缺血再灌注损伤中的作用仍研究不足。
实验中，采用TTC染色评估心肌活力，利用心脏超声测量左心室射血功能。通过形态学染色和心肌损伤标志物检测评估心脏损伤。采用透射电子显微镜观察心肌组织中的线粒体形态，并进行ELISA检测以评估线粒体复合物的活性。利用腺相关病毒敲低技术验证Nrf2的作用。在实验中，使用共聚焦显微镜扫描心肌细胞中的线粒体形态，并观察Nrf2分子的细胞内定位。
TTC染色显示，心肌缺血再灌注损伤显著增加了左心室梗死面积，而用YWPC（黄酒多酚化合物）预处理可显著减小梗死面积。心脏超声表明，YWPC干预可保留左心室射血分数。形态学染色和心肌损伤标志物检测显示心肌缺血再灌注损伤导致组织水肿，增加心肌细胞凋亡和损伤，但YWPC预处理减轻了这些损伤。透射电子显微镜显示YWPC逆转了心肌缺血再灌注损伤引起的过度线粒体分裂。免疫荧光表明YWPC显著促进Nrf2核转位并增加下游抗氧化分子的表达。
YWPC预处理可通过减少心肌缺血再灌注损伤诱导的过度线粒体分裂来保护心肌组织，且Nrf2介导这些作用。
