Inhibition of NF-κB activity by 15d-PGJ₂ in A2780 and doxorubicin A2780/AD cells.

<p>To measure NF-κB activity, both A2780 and A2780/AD cells were transiently transfected with a plasmid containing the NF-κB promoter with a luciferase reporter element (pNF-κB-Luc) for 24 h. After 24 h, 15d-PGJ₂, ciglitazone or BAY-11-7082 were incubated with and without TNF-α for 4 h and then luciferase activity was measured using a luminescence assay to determine the NF-κB activity. (<b>A</b>) The NF-κB pathway activator, TNF-α (100 ng/ml), induced the NF-κB activity in both cell types although the increase was higher in A2780 cells. Treatment with 15d-PGJ₂ significantly inhibited NF-κB activity in both A2780 (<b>B</b>) and A2780/AD cells (<b>C</b>) which was more pronounced in TNF-α−activated cells. Ciglitazone inhibited NF-κB only at higher concentrations or in TNF-α−activated A2780/AD cells. BAY-11-7082 inhibited the NF-κB activity in both cell types with similar efficacy. Data represent the average of at least 3 separate experiments. Statistical differences versus the respective controls are shown as *<i>p</i><0.05 and **<i>p</i><0.01.