Skip to main content
. 2015 Jun 11;11(8):970–981. doi: 10.7150/ijbs.11635

Figure 3.

Figure 3

DT-13 inhibited TNF-α-induced ICAM-1 & VCAM-1 activity dependent with NF-κB pathway. (A). DT-13 inhibited TNF-α-induced p-65 phosphorylation in HUVECs. HUVECs were pretreated with DT-13 (0.01, 0.1 or 1 μM) for 1 h followed by TNF-α (10 ng/mL) exposure. Expression and activation of p-65 were detected by western blotting. ## P<0.01 νs. the control group; * P<0.05,** P<0.01 νs. the TNF-α group. (B) & (C). The over-expression of p65 overcomes the inhibitory effect of DT-13 on ICAM-1 (B) and VCAM-1 (C) expression. (D) Human ICAM-1 promoter or (E) VCAM-1 promoter were ligated into pGL3 basic luciferase vectors. The binding sites for transcription factors are also shown. Right: Cells were transfected with indicated forms of (D) ICAM-1 or (E) VCAM-1 promoter for 24 h, and then incubated with DT-13 for 1 h followed by TNF-α (10 ng/mL) stimulation for 4 h. The promoter activity is represented by the level of luciferase activity indicated by relative light units (RLU). pRL-TK plasmid was also transfected into cells and used as an internal control. The data represent the mean ± SD of three experiments. # P<0.05, ## P<0.01 νs. the control group; * P<0.05,** P<0.01 νs. the TNF-α group.