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. 2019 Nov 12;9:16636. doi: 10.1038/s41598-019-53305-z

Figure 6.

Figure 6

ALA enhanced hPXR-mediated NF-κB-luciferase activity inhibition, activated the wild-type hPXR but not the mutant hPXR. (A) HT-29 cells were electroporated with the hPXR expression vector pSG5-hPXR or the control vacuum vector. Cells were subjected to western blot analysis to determine protein expression (Left panel) or subjected to NF-κB reporter assay as described in Methods (Right panel). (B) HT-29 cells were co-transfected with CYP3A4-luciferase reporter combined with pRL-TK, and the wild-type hPXR expression construct (pSG5-hPXR) or the double-mutant (S247W/C284W) hPXR construct or the triple-mutant (S247W/C284W/S208W) hPXR construct. Cells were incubated with ALA (25 μM) or rifampicin (10 μM) for 24 h. Cell extracts were assayed for luciferase activity. The results were expressed as fold induction of the vehicle-treated cells. Data are presented as the mean ± SD of three independent experiments. ***p < 0.001 vs. control cells; ##P < 0.01, ###P < 0.001 vs. LPS alone treatment cells.