Inhibitory effect of aloperine on transient outward potassium currents in rat cardiac myocytes

• Published in: Frontiers in pharmacology Vol. 15; p. 1372973
• Main Authors: Dong, Xiao-Na, Li, Meng-Ting
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 28.03.2024
• Subjects: aloperine; atrial fibrillation; molecular docking; Pharmacology; transient outward potassium current; whole-cell patch-clamp; atrial fibrillation; aloperine; molecular docking; whole-cell patch-clamp; transient outward potassium current
• ISSN: 1663-9812; 1663-9812
• DOI: 10.3389/fphar.2024.1372973

Aloperine (ALO) is an effective quinolizidine alkaloid. Previous research has demonstrated its antiarrhythmic effect by inhibiting voltage-gated sodium currents in rat ventricular myocytes. This study explored its effect on transient outward potassium currents (I ) in rat atrial myocytes to identify potential targets in the context of ion channel currents. The I characteristics in rat atrial myocytes were recorded using a whole-cell patch-clamp technique. Molecular docking was performed to validate ligand-protein binding interactions. ALO at concentrations of 3 and 10 μM significantly reduced I current densities. Gating kinetics analysis revealed ALO's ability to slow I activation, hasten inactivation, and prolong transition from inactive to resting state. Molecular docking revealed that ALO could stably bind to . ALO may inhibit I by slowing the activation process, accelerating inactivation, and delaying the recovery time after inactivation, potentially preventing acetylcholine-induced AF.