Brilliant blue G enhances cardiac function and suppresses ventricular arrhythmias by attenuating inflammation and fibrosis after post-myocardial infarction in rats.

Myocardial infarction (MI) is a leading cause of heart failure and ventricular arrhythmias, driven by excessive inflammation and adverse cardiac remodeling. The purinergic P2X7 receptor (P2X7R) plays a critical role in acute MI, however, the long-term effect of P2X7R on chronic MI and arrhythmia remains unknown. This study investigated the effects of long-term modulation of P2X7R on inflammation, fibrosis, and arrhythmias in a rat model of MI. Male Sprague-Dawley rats underwent left anterior descending coronary artery ligation and were assigned to sham, MI, MI + Brilliant Blue G (BBG, P2X7R antagonist), or MI + BzATP (P2X7R agonist) groups for 28 days. BBG treatment significantly reduced ventricular tachycardia induction rates, shortened QT, QTc, and Tpeak-Tend intervals, and improved cardiac function, as evidenced by increased ejection fraction, fractional shortening, and cardiac output. Histological analyses revealed reduced inflammatory cell infiltration, necrosis, and collagen deposition in the MI + BBG group compared to MI groups. ELISA confirmed that BBG lowered pro-inflammatory cytokines TNF-α, IL-1β and TGF-β1 levels. P2X7 mRNA expression was attenuated by BBG, but not significantly altered. These findings demonstrate that BBG mitigates post-MI inflammation, fibrosis, and arrhythmias while enhancing cardiac function.