Skip to main content
Figure 3 | Critical Care

Figure 3

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

Figure 3

Dobutamine promotes TNF-α expression and phosphorylation of IκBα, p38 mitogen-activated protein kinase (MAPK) and c-jun NH2-terminal kinase (JNK) in lipopolysaccharide (LPS)-treated cardiomyocytes. Adult mouse ventricular myocytes were treated with dobutamine (DOB, 0.02 μM), LPS (10 ng/mL), their combination, or vehicle for 6 hours and 12 hours. The total cardiomyocyte lysates and nuclear proteins were prepared. (A) The expression of TNF-α in cardiomyocytes was detected by western blot (mean ± standard error of the mean (SEM); n = 6). (B) NF-kB p65 DNA binding activity in nuclear proteins was examined using Cayman’s NF-kB (p65) Transcription Factor Assay kit, and is expressed as percent changes relative to control (mean ± SEM; n = 6). The levels of p-IκBα/IκBα (C), p-ERK/ERK (D), p-p38 MAPK/ p38 MAPK (E) and p-JNK/JNK (F) were examined by western blotting of whole cell lysates with specific antibodies, respectively (mean ± SEM; n = 3). * P <0.05 compared with the control group; # P <0.05; ## P <0.01 compared with the LPS group.

Back to article page