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Objective To investigate the role of c-Jun NH2-terminal kinase (c-JNK) signaling pathway on voltage-gated potassium channel (Kv) remodeling in left ventricular myocytes of diabetic rats, and explore the intrinsic regulatory mechanism. Methods Forty-five SD rats were randomly divided into DM group (n=25, modeling with streptozotocin induction) and control group (n=20, fed with normal diet). Transient outward potassium current (Ito) of rats' ventricular myocytes in DM group and control group was recorded by whole-cell patch-clamp method. The c-Jun activity was detected using a non-radioactive JNK kinase assay kit (Cell Signaling Technology). JNK inhibitor SP600125 was used to incubate the cardiomyocytes of diabetes rats in vitro, and then the changes of Ito in cardiomyocytes were observed. Thioredoxin reductase (TrxR) inhibitor--auranofin (AF) was used to treat the rats' cardiomyocytes incubated with SP600125, and then the changes of Ito in cardiomyocytes were observed. The content of Kv4.2 was tested using anti-Kv4.2 antibody, and the results were analyzed using a UVP bioimaging system. Results The JNK activity in DM group rose more than 1 times compared with control group, while the density of Ito decreased significantly (Control: 30.2±3.3pA/pF, n=16; DM: 15.3±2.1pA/pF, n=17; P