Abstract
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 (n = 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.
Keywords
apelin-36 - biomarker - heart failure - oxidative stress - MDA - GSH - protein carbonyl
