Figure 2.
Figure 2. Effect of blocking NF-κB activation on IL-1β and endotoxin-induced TM repression. HUVECs were pretreated with 8 μM parthenolide or transduced with either AdNull or AdIκBsr (MOI = 100 pfu/cell) prior to stimulation without (▪) or with 10 ng/mL human IL-1β (A, ▦)or10 μg/mL bacterial endotoxin (B, ▦) for 16 hours. TM gene expression, normalized to CD31, was determined by real-time PCR. Values shown are the mean ± SEM of 3 experiments (n = 6 for control groups). *P < .01 for parthenolide compared with control groups stimulated with IL-1β or endotoxin. #P ≤ .001 for AdIκBsr compared with AdNull or control groups stimulated with IL-1β or endotoxin.

Effect of blocking NF-κB activation on IL-1β and endotoxin-induced TM repression. HUVECs were pretreated with 8 μM parthenolide or transduced with either AdNull or AdIκBsr (MOI = 100 pfu/cell) prior to stimulation without (▪) or with 10 ng/mL human IL-1β (A, ▦)or10 μg/mL bacterial endotoxin (B, ▦) for 16 hours. TM gene expression, normalized to CD31, was determined by real-time PCR. Values shown are the mean ± SEM of 3 experiments (n = 6 for control groups). *P < .01 for parthenolide compared with control groups stimulated with IL-1β or endotoxin. #P ≤ .001 for AdIκBsr compared with AdNull or control groups stimulated with IL-1β or endotoxin.

Close Modal

or Create an Account

Close Modal
Close Modal