Ferdinal Frans, Limanan David, Rini Retno Dwi, Alexsandro Rio, Helmi Rizal
Department of Biochemisty and Molecular Biology, School of Medicine, Tarumanagara University, Jakarta, Indonesia.
Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Indonesia, Jakarta Pusat, Indonesia.
Int J Angiol. 2019 Sep;28(3):194-199. doi: 10.1055/s-0038-1676340. Epub 2018 Dec 20.
Apelin is a novel adipokine identified as an endogenous ligand of the specific orphan receptor APJ. Among the various isoforms of apelin, an increase in the apelin-36 plasma level has been associated with oxidative stress, and this isoform has various biological effects, such as positive inotropic, vasodilatory, and antiatherosclerotic effects. Therefore, apelin-36 may be used as a biomarker of heart failure (HF). Advances in the understanding of the molecular mechanisms underlying HF cannot be achieved without the use of animal models. However, it is unclear whether chronic systemic hypoxia can cause HF in rats. The present study aimed to determine whether chronic systemic hypoxia can cause HF in rats and whether apelin-36 can be used as a biomarker of HF. The study included Sprague-Dawley rats. The rats were randomly divided into seven groups ( = 4). One of the groups was a control group, and the six other groups were exposed to hypoxia (8% O2) for different durations (6 hours, 1 day, 3 days, 5 days, 7 days, and 14 days). The exposure groups showed ventricular hypertrophy accompanied by myocardial structural damage, which indicated ventricular remodeling. In addition, the exposure groups showed elevated apelin-36 plasma levels and signs of oxidative stress. Moreover, gel electrophoresis of heart tissue showed five bands that corresponded to apelin isotypes, including apelin-36. In an experimental rat HF model with chronic systemic hypoxia, apelin-36 was elevated along with oxidative stress. Apelin-36 along with oxidative stress may serve as a biomarker of HF in this model.
阿片肽是一种新发现的脂肪因子，被确定为特定孤儿受体APJ的内源性配体。在阿片肽的各种异构体中，血浆阿片肽-36水平的升高与氧化应激有关，并且这种异构体具有多种生物学效应，如正性肌力、血管舒张和抗动脉粥样硬化作用。因此，阿片肽-36可作为心力衰竭（HF）的生物标志物。如果不使用动物模型，就无法在理解HF潜在分子机制方面取得进展。然而，尚不清楚慢性全身性缺氧是否会导致大鼠发生HF。本研究旨在确定慢性全身性缺氧是否会导致大鼠发生HF，以及阿片肽-36是否可作为HF的生物标志物。该研究包括Sprague-Dawley大鼠。大鼠被随机分为七组（每组n = 4）。其中一组为对照组，其他六组分别暴露于不同时长的缺氧环境（8%氧气）中（6小时、1天、3天、5天、7天和14天）。暴露组出现心室肥厚并伴有心肌结构损伤，这表明发生了心室重构。此外，暴露组的血浆阿片肽-36水平升高且有氧化应激迹象。而且，心脏组织的凝胶电泳显示出五条与阿片肽异构体相对应的条带，包括阿片肽-36。在慢性全身性缺氧的实验性大鼠HF模型中，阿片肽-36随着氧化应激而升高。在该模型中，阿片肽-36与氧化应激一起可能作为HF的生物标志物。
