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. Author manuscript; available in PMC: 2011 Mar 14.
Published in final edited form as: Hepatology. 2008 Nov;48(5):1632–1643. doi: 10.1002/hep.22519

Figure 4. Activation of FXR antagonizes the NF-κB transactivity.

Figure 4

(A, B) Relative luciferase activities of HepG2 cells that were co-transfected with the NF-κB reporter plasmids, the control plasmid phRL-TK, and/or FXR/RXR expression plasmids. Cells were pre-treated with GW4064 or vehicle (DMSO) for 18 h before treatment with TPA (50nM) or LPS (1 μg/ml) for 6 h. *P < .05 compared to the groups of TPA or LPS treatment without transfection of FXR/RXR plasmids (n=3). (C) Relative luciferase activities of HepG2 cells that were co-transfected with the NF-κB reporter plasmids, the control plasmid phRL-TK, and increasing amounts of FXR/RXR at 0.5:1, 1:1, 2:1 or 3:1 ratios with the p65 expression plasmid. Cells were treated with GW4064 or vehicle (DMSO) for 24 h. **P < .005 compared to the group of p65 overexpression with GW4064 treatment (n=3).