Key result
CPU 86017 inhibited IKur in a concentration-dependent manner (IC50 4.56 and 0.21 μmol/L) and prolonged atrial effective refractory period by 38.9% in experimental atrial fibrillation rat models.
CPU 86017 exhibits anti-atrial fibrillation properties in preclinical models by inhibiting IKur currents and prolonging the atrial effective refractory period.
Aim Compared with azimilide, the present study was designed to observe the anti-atrial fibrillation (AF) effects of CPU 86017, a berberine derivative, and explore its possible ion-channel mechanism. Methods The effects of CPU 86017 on ultra-rapid delayed rectifier K + current ( I Kur ) was studied both on guinea pigs atrial cardiomyocytes and human embryonic kidney (HEK) 293 cell line with whole-cell patch clamp technique. Anti-AF action of CPU 86017 (1.25, 2.5 mg·kg −1 , ip) was observed in AF model rats induced by acetylcholine (ACh)-CaCl 2 . Results CPU 86017 inhibited I Kur in a concentration-dependent manner. The IC 50 of I Kur on atrial myocytes and HEK293 cells was 4.56 and 0.21 μmol·L −1 , respectively. On the AF rats, CPU 86017 effectively shortened AF duration, prolonging atrial effective refractory period (AERP) by 38.9% in rats atrial. Conclusion CPU86017 inhibited I Kur in a concentration-dependent manner. It was effective in treating AF partly by inhibiting I Kur and prolonging AERP.
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Tang et al. (2010) studied Atrial fibrillation. CPU 86017 vs. Azimilide was evaluated on IKur current inhibition and atrial effective refractory period (AERP) prolongation. CPU 86017 inhibited IKur in a concentration-dependent manner (IC50 4.56 and 0.21 μmol/L) and prolonged atrial effective refractory period by 38.9% in experimental atrial fibrillation rat models.
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