Pinocembrin attenuates autonomic dysfunction and atrial fibrillation susceptibility via inhibition of the NF-κB/TNF-α pathway in a rat model of myocardial infarction.

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.