Cardiac fibrosis and inflammation play critical roles in ventricular remodelling after myocardial infarction (MI). Urolithin B (UB), a metabolite of ellagitannin-rich foods, has various biological activities, but its effect on ventricular remodelling after MI has not been determined. The present study evaluated whether UB inhibited ventricular structural remodelling and decreased the occurrence of ventricular arrhythmias after MI. Sprague-Dawley (SD) rats underwent ligation of the left anterior descending coronary artery before randomization to receive phosphate-buffered saline (PBS) or UB at doses of 2.5 mg/kg/day and 5 mg/kg/day via intraperitoneal administration or sham ligation. Cardiac function was assessed using echocardiography, haemodynamic detection and brain natriuretic peptide (BNP) levels 2 weeks post-MI. Hearts were used for electrophysiological testing and molecular and histological analyses. UB (5 mg/kg/day) significantly protected against post-MI cardiac dysfunction. UB markedly reduced infarct areas and myocyte size and attenuated cardiac fibrosis and inflammation post-MI. UB decreased the incidence of ventricular tachycardia and ventricular fibrillation compared to the MI group. We determined that UB inhibited the phosphorylation of JAK2/STAT3 and Smad2/3 signalling molecules. Our data suggest that UB reduces the occurrence of malignant ventricular arrhythmias after MI, which is likely associated with attenuation of ventricular structural remodelling via inactivation of the JAK2/STAT3 and Smad2/3 signalling pathway.
Keywords: Cardiac function; Myocardial infarction; Urolithin B; Ventricular arrhythmia.
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