Endothelin-NADPH oxidase mediates cardiomyocytes dysfunction caused by H₂O₂ and interventions by CPU0213

Over-activated NADPH oxidase and endothelin（ET）system are the main mechanism of cardiomyocytes dysfunction.This research mainly focuses on the hypothesis that CPU0213 attenuates cardiomyocytes dysfunction by inhibiting the over-expression of ET-NADPH oxidase.Cardiomyocytes were divided into groups:control, H₂O₂ group, H89/Bis, APO/DPI, CPU0213 group.The expression of FKBP12.6, SERCA2a and CASQ2 were down-regulated and pPKCε/PKCε，NADPH oxidase and ET_AR/ET_BR were up-regulated in H₂O₂ treated group,which implyed the involvement of PKCε.Endothelin receptor antagonist CPU0213 attenuated the abnormal expression of FKBP12.6, SERCA2a and CASQ2 by inhibiting pPKC-NADPH pathway.