Table 6.

The mechanisms of allicin in arrhythmias

Research model	Model establishment	Intervention methods	Drug effects	Main molecular mechanisms	Citation
Human atrial myocytes	–	30 μmol/l for 3 min (validation concentration)	Prolonging the action potential duration	⬇ Ito	[72]
Ventricular cardiac myocytes from C57BL/6	–	10, 30, 100, and 300 μmol/l for 5 min at a rate of 2‑3 ml/min at room temperature	Anti-arrhythmia	⬇ Ito	[73]
Primary cardiomyocytes from neonatal Sprague–Dawley rats	–	3, 10, 30 μmol/l for 48 h	Anti-arrhythmia	⬇ Cav1.2 channel protein trafficking	[75]
HEK293 with△KPQ-SCN5A mutations	The transferred △KPQ-SCN5A plasmid was transiently	30 μmol/l (validation concentration)	Increasing the channel steady-state and intermediate-state inactivation, reducing the window current	⬇ INa, L, INa, L/INa, P ⬆ Nav1.5 channel protein	[76]

Cav1.2: the l-type calcium; △KPQ-SCN5A: the cardiac Na⁺ channel; I_{Na, L}: the late sodium current; I_{Na, P}: persistent sodium current; I_to: transient outward potassium current