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. 2013 Aug 27;170(2):403–414. doi: 10.1111/bph.12284

Figure 5.

Figure 5

Isoform-selective activation of hCAR-SV23, hCAR-SV24, and hCAR-WT by 3-hydroxyflavone. Cultured HepG2 cells were transfected with pCMV6-XL4-hRXRα (except for the hCAR-WT assay), pGL4.74[hRluc/TK] internal control vector, pGL3-basic-CYP2B6-PBREM/XREM-luc, and a receptor expression plasmid or its respective empty vector, as described under Methods. The receptor expression plasmids were (A) pCMV6-neo-hCAR-SV23, (B) pCMV6-XL4-hCAR-SV24, and (C) pCMV6-XL4-hCAR-WT. Transfected cells were treated with DMSO (0.1% v/v; vehicle) or 3-hydroxyflavone (1–30 μM). In the hCAR-WT-dependent reporter gene assay, androstanol (10 μM; inverse agonist of hCAR-WT) was added to each treatment group. Firefly luciferase and R. reniformis luciferase activities were quantified and normalized as described under Methods. Data are expressed as mean ± S.E.M. for three or four independent experiments performed in triplicate. *, significantly different from the same treatment group transfected with the empty vector and the vehicle-treated control group transfected with the same receptor expression plasmid (P < 0.05).