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Figure 6 | Critical Care

Figure 6

From: β1-adrenoceptor stimulation promotes LPS-induced cardiomyocyte apoptosis through activating PKA and enhancing CaMKII and IκBα phosphorylation

Figure 6

Effects of dobutamine (DOB), lipolysachharide (LPS) and nifedipine (NIF) on cytosolic Ca2+ , calmodulin-dependent protein kinase II (CaMKII) and caspase activation in cardiomyocytes. Adult mouse ventricular myocytes were pretreated with NIF (1 μM), a calcium channel blocker, or vehicle for 1 hour, and then exposed to DOB (0.02 μM), LPS (10 ng/mL), their combination or vehicle for 3, 12 or 24 hours. (A,B) DOB enhanced LPS-induced cytosolic Ca2+ concentration elevation (mean ± standard error of the mean (SEM); n = 8) and calmodulin-dependent protein kinase II (CaMKII) phosphorylation (mean ± SEM; n = 4) 3 hours and 12 hours after LPS treatment, respectively, both of which were blocked by NIF pretreatment. (C,D) NIF partly abolished the enhancement effects of DOB on LPS-stimulated caspase-9 (12 hours after DOB and LPS treatment) and caspase 3/7 (24 hours after DOB and LPS treatment) activation in cardiomyocytes (mean ± SEM; n = 8). * 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.

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Critical Care

ISSN: 1364-8535