Curcumin Inhibits HERG Potassium Channels In Vitro

Object: Curcumin is reported to exert antioxidant, anti-inflammatory, antiviral,antibacterial, antifungal, and anti-tumor activities. The human ether-a-go-go relatedgene (hERG) encodes the rapid component of the delayed rectifier K+currents.Inhibition of hERG K+channels leads to cardiac repolarization prolongation, whichcontributes to either the anti-arrhythmic effects of anti-arrhythmic drugs, or thepro-arrhythmic effects (induction of long QT syndrome) of some drugs not used foranti-arrhythmias. Since curcumin shows multiple beneficial effects and clinicalsignificance, the aim of the present study is to investigate the effect of curcumin onhERG K+channels, elucidating its potential cardiac therapeutic or toxic effects.Method：(1) Effects of curcumin on hERG K+currents were investigated bypatch-clamp technique.(2) MTT assay was used to assess the effects of curcumin onviability of cells.(3) Effects of curcumin on cardiac repolarization of New Zealandwhite rabbits were monitored by BL-420E+bio-function experimental system afteranimals were injected with curcumin intravenously.Result： In whole-cell patch-clamp experiments, we found that curcumininhibited hERG K+currents in HEK293cells stably expressing hERG channels in adose-dependent manner, with IC50value of5.55μM. The deactivation, inactivationand the recovery time from inactivation of hERG channels were significantly changedby acute treatment of10μM curcumin. Incubation of20μM curcumin for24hrsreduced the HEK293cell viability. Intravenous injection of maximal amount ofcurcumin in rabbits (20mg/animal) did not affect the cardiac repolarization manifestedwith QTc value.Conclusion: Curcumin inhibits hERG K+channels in vitro and has no effects oncardiac repolarization in vivo.