Propofol Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor-Alpha Expression and Myocardial Depression through Decreasing the Generation of Superoxide Anion in Cardiomyocytes
Figure 4
The inhibitory effect of propofol on ERK1/2 and p38 phosphorylation in LPS-stimulated cardiomyocytes. Cardiomyocytes were pretreated with vehicle, DPI (50 μM), or propofol (50 μM) followed by LPS (4 μg/mL) for 2 hours. (a) The effect of propofol or DPI on ERK1/2 phosphorylation. (b) The effect of propofol or DPI on p38 phosphorylation. (c) Gray intensity analysis of the western blot results of ERK1/2 phosphorylation. (d) Gray intensity analysis of the western blot results of p38 phosphorylation. Cardiomyocytes were pretreated with vehicle, PD98059 (20 μM), or SB203580 (10 μM) followed by LPS (4 μg/mL) for 4 hours. (e) TNF-α protein measurement by ELISA at 4 hours after LPS treatment; (f) TNF-α mRNA measurement by real time RT-PCR at 2 hours after LPS treatment (each bar represents the mean ± S.D, , compared with LPS group; ).
