Laboratory of Centre for Preclinical Research, Department of Experimental and Clinical Physiology, Medical University of Warsaw, Warsaw, Poland.
Centre of Postgraduate Medical Education, Department of Urology, Warsaw, Poland.
PLoS One. 2024 Sep 18;19(9):e0308833. doi: 10.1371/journal.pone.0308833. eCollection 2024.
Myocardial infarction (MI) significantly contributes to the global mortality rate, often leading to heart failure (HF) due to left ventricular remodeling. Key factors in the pathomechanism of HF include nitrosative/oxidative stress, inflammation, and endoplasmic reticulum (ER) stress. Furthermore, while a high-fat diet (HFD) is known to exacerbate post-MI cardiac remodeling, its impact on these critical factors in the context of HF is not as well understood.
This study aimed to assess the impact of post-MI HF and HFD on inflammation, nitro-oxidative stress, ER stress, and unfolded protein response (UPR).
The study was performed on fragments of the left ventricle harvested from 30 male adult Sprague Dawley rats, which were divided into four groups based on diet (normal-fat vs. high-fat) and surgical procedure (sham operation vs. coronary artery ligation to induce MI). We assessed body weight, NT-proBNP levels, protein levels related to nitrosative/oxidative stress, ER stress, UPR, apoptosis, and nitric oxide synthases, through Western Blot and ELISA.
HFD and MI significantly influenced body weight and NT-proBNP concentrations. HFD elevated 3-nitrotyrosine and myeloperoxidase levels and altered nitric oxide synthase levels. HFD and MI significantly affected ER stress markers and activated or inhibited UPR pathways.
The study demonstrates significant impacts of post-MI HF and dietary fat content on cardiac function and stress markers in a rat model. The interaction between HFD and MI on UPR activation suggests the importance of dietary management in post-MI recovery and HF prevention.
心肌梗死（MI）显著导致全球死亡率，常因左心室重构导致心力衰竭（HF）。HF 的发病机制中的关键因素包括硝化/氧化应激、炎症和内质网（ER）应激。此外，虽然高脂肪饮食（HFD）已知会加重 MI 后心脏重构，但它对 HF 中这些关键因素的影响尚未得到很好的理解。
本研究旨在评估 MI 后 HF 和 HFD 对炎症、硝化/氧化应激、ER 应激和未折叠蛋白反应（UPR）的影响。
该研究在 30 只雄性成年 Sprague Dawley 大鼠的左心室片段上进行，这些大鼠根据饮食（正常脂肪与高脂肪）和手术程序（假手术与冠状动脉结扎以诱导 MI）分为四组。我们通过 Western Blot 和 ELISA 评估了体重、NT-proBNP 水平、与硝化/氧化应激、ER 应激、UPR、凋亡和一氧化氮合酶相关的蛋白质水平。
HFD 和 MI 显著影响体重和 NT-proBNP 浓度。HFD 升高了 3-硝基酪氨酸和髓过氧化物酶水平，并改变了一氧化氮合酶水平。HFD 和 MI 显著影响 ER 应激标志物并激活或抑制 UPR 途径。
该研究表明，MI 后 HF 和饮食脂肪含量对大鼠模型中心脏功能和应激标志物有显著影响。HFD 和 MI 对 UPR 激活的相互作用表明在 MI 后恢复和 HF 预防中饮食管理的重要性。
