Curcumin inhibits hERG potassium channels in vitro

Curcumin is reported to exert antioxidant, anti-inflammatory, antiviral, antibacterial, antifungal, and anti-tumor activities. The human ether-a-go-go related gene (hERG) encodes the rapid component of the delayed rectifier K+ currents. Inhibition of hERG K+ channels leads to cardiac repolarization prolongation, which contributes to either the anti-arrhythmic effects of anti-arrhythmic drugs, or the pro-arrhythmic effects (induction of long QT syndrome) of some drugs not used for anti-arrhythmias. Since curcumin shows multiple beneficial effects and clinical significance, the aim of the present study is to investigate the effect of curcumin on hERG K+ channels, elucidating its potential cardiac therapeutic or toxic effects. In whole-cell patch-clamp experiments, we found that curcumin inhibited hERG K+ currents in HEK293 cells stably expressing hERG channels in a dose-dependent manner, with IC50 value of 5.55 μM. The deactivation, inactivation and the recovery time from inactivation of hERG channels were significantly changed by acute treatment of 10 μM curcumin. Incubation of 20 μM curcumin for 24 h reduced the HEK293 cell viability. Intravenous injection of maximal amount of curcumin in rabbits (20 mg/animal) did not affect the cardiac repolarization manifested with QTc value. We conclude that curcumin inhibits hERG K+ channels in vitro.

► Curcumin inhibited hERG K+ channels expressed in HEK293 cells. ► Curcumin accelerated the deactivation and inactivation of hERG channels. ► Intravenous injection of maximal amount of curcumin did not affect QTc in rabbits.