Fig. 3.

CINPA1 is a weak antagonist of PXR, but it does not modulate the activity of other nuclear receptors. (A) HepG2-PXR Clone 1 cells were treated with DMSO or 18 µM of CINPA1 in the presence or absence of 5 µM rifampicin for 24 hours before luciferase assay using Steadylite. (B–I) GeneBLAzer cells were plated according to the manufacturer’s instructions and treated with DMSO (control), a predetermined concentration of the indicated nuclear receptor (NR) antagonist (as detailed in the description of our experimental procedures), or 18 µM of CINPA1. NR-mediated β-lactamase activity was measured as a FRET ratio after 24-hour treatment. Data are presented as % Activity, determined by setting the maximum FRET signal obtained for each receptor (in the respective agonist + DMSO wells) to 100%. One-way analysis of variance with Bonferroni corrections for multiple comparisons was used to analyze data (as noted in brackets), and statistical significant differences are indicated by *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant, P > 0.05. eGugg, Guggulsterone; Feno, Fenofibrate; GW9, GW9662; 22HC, 22(S)-hydroxycholesterol; 9-cis RA, 9-cis retinoic acid.