Previous studies indicate that
myocardial infarction (MI) may contribute to
atrial fibrillation (AF). Emerging evidence has shown that
pinocembrin protects myocardial ischemic injury (I/R)-induced cardiac
fibrosis and arrhythmias in animals via its anti-inflammatory or
antioxidant activities. However, the effects of
pinocembrin on MI-induced atrial arrhythmias remain unknown. Thus, this study aimed to investigate the effects of
pinocembrin on autonomic dysfunction and AF susceptibility in MI rats and the possible mechanism. In a standard experimental MI model, Sprague-Dawley rats received permanent
ligation of the left anterior descending (LAD) coronary artery and were treated with
pinocembrin or saline for 6 days. Our results demonstrated that
pinocembrin treatment significantly decreased sympathetic activity, augmented parasympathetic activity, improved heart rate variability (HRV), prolonged the atrial effective refractory period (ERP) and action potential duration (APD), shortened activation latency (AL), lowered the indicibility rate of AF, attenuated atrial
fibrosis, and decreased concentrations of
norepinephrine (NE),
tumor necrosis factor-α (TNF-α),
interleukin (IL)-1β and
IL-6 in the serum and the left atrial (LA). Furthermore,
pinocembrin treatment significantly increased the expression levels of
Cx43 and Cav1.2 and suppressed the phosphorylation of inhibitor-κBα (IκBα) and the activation of
nuclear factor-kappa B (NF-κB)subunit p65. In conclusion, the findings indicate that
pinocembrin treatment decreases autonomic remodeling, lowers atrial
fibrosis, ameliorates atrial
electrical remodeling, and suppresses MI-induced inflammatory responses, which suggests a potential novel strategy for atrial arrhythmias.