Fig. 5.

Transcription activation of P3 by retinoic acid receptor α (RARα), RAR-related orphan receptor α (RORα), constitutive androstane receptor (CAR), pregnane X receptor (PXR), and aryl hydrocarbon receptor (AhR). HepG2 cells were co-transfected for 12 h with a total of 2 μg of plasmid DNA containing 1 μg of pGL3-3kbP3-Luc, an increasing amount of pCMX-hRORα, pTARGET-hAhR, pCMV-hCAR, pCMV-hPXR, or pCMX-hRAR (0, 0.2, 0.4, 0.8, or 1 μg) and a decreasing amount of empty vector (1, 0.8, 0.6, 0.2, or 0 μg). The transfected cells were then cultured in serum-containing medium for additional 24 h followed by 24 h treatment with activators appropriate to individual nuclear receptor at appropriate concentration of melatonin (100 μM), 3-methylcholanthrene, (5 μM), 6-(4-chlorophenyl)imidazole(2,1-b)(1,3)thiazole-5-carbaldehyde O-(3,4-dichloronezyl)oxime (1 μM), refampicin (10 μM), or 9-cis-retinoic acid (1 μM). Cell extracts were prepared and luciferase activity was determined. Values represent the mean ± SD of three independent transfections. *p ≤ 0.05; **p ≤ 0.01, significantly different from cells transfected with empty vector without nuclear receptor gene