ASSA13-03-15 The Role of P66shc Adapter Protein in the Inhibitory Action of Curcumin on Cardiomyocyte Apoptosis Induced by AngII

Objective To explore the role of p66shc adapter protein in the cardiomyocyte apoptosis induced by AngII, and the effects of curcumin pretreatment. Methods Neonatal rat cardiomyocytes (NRCMs) were prepared from 1 to 2 days old Sprague-Dawley rats, and were randomly divided into five groups, including normal control group, 10 –11 M AngIIgroup, 10 –9 M AngIIgroup, 10 –7 M AngIIgroup, and 10 –7 M AngII+curcumin group. The cell viability was measured by MTT. The level of reactive oxygen species (ROS) in the whole cell and cell apoptosis rate were measured by the flow cytometry. Mitochondrial membrane potential (MMP) was detected using a fluorescence microplate reader, and the protein expression of phosphorylated and total p66shc was detected using western blot. Results With the increasing AngIIconcentration on NRCMs, cell viabilities and MMP levels were gradually decreased, and the levels of ROS in the cardiomyocytes and the cell apoptosis rates were both increased (P Conclusions p66shc plays an important role in the cardiomyocyte apoptosis induced by AngII, and curcumin could attenuate AngII induced cardiomyocyte injury through down-regulating the protein expression of p66shc.