Celastrol, a bioaetive compound extracted from Tripterygium wilfordii Hook F., has recently attracted much attention for its potential in multiple applications, such as anti-inflammation use, degenerative neuron disease relief and tumor management.Notably, it has been reported that celastrol exerts inhibitory effects on surface expression of hERG and Kir2.1 potassium channels heterologously expressed in HEK293 cells and affects the normal development of zebrafish embryo in μM concentrations, suggesting its potential toxicity.Thus, the present study was designed to investigate the cardiotoxicity of celastrol.The preliminary results showed that chronic incubation with celastrol at concentration of 400nM significantly caused a prolongation of the action potential duration (APD), which coordinately associated with the reduction in Ikr as well as Ik1 and Ito in neonatal rat ventricular myocytes (NRVMs).