Figure 5

Effects of KT5720, a protein kinase A (PKA) inhibitor, on apoptosis-associated molecules in dobutamine (DOB) and lipolysaccharide (LPS)-treated cardiomyocytes. Adult mouse ventricular myocytes were pretreated with KT5720 (5 μM) or vehicle for 1 hour, and then exposed to DOB (0.02 μM), LPS (10 ng/mL), their combination, or vehicle for 12 hours. Caspase-8 (A) and caspase-9 (C) activities were detected 12 hours after DOB and LPS treatment (mean ± standard error of the mean (SEM); n = 8). IκBα (B), p38 mitogen-activated protein kinase (MAPK) (D) and c-jun NH2-terminal kinase (JNK) (E) phosphorylation, as well as Bcl-2 (F) protein expression in cardiomyocytes, were also examined 12 hours after DOB and LPS treatment using western blotting (mean ± SEM; n = 3). The results showed that KT5720 reversed the effects of dobutamine (DOB) on caspase-9 activation, Bcl-2 expression as well as p38 MAPK and JNK phosphorylation, but not on caspase-8 activation and IκBα phosphorylation in LPS-challenged cardiomyocytes. ^* P <0.05 compared with the control group; ^# P <0.05 compared with the LPS group; ^▲ P <0.05 compared with the DOB plus LPS group.