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. 2017 Mar 30;8:162. doi: 10.3389/fphar.2017.00162

FIGURE 7.

FIGURE 7

Target selectivity of compound 2. (A) HepG2 cells were transiently transfected with p(UAS)9XTKLuc, pSG5-PPARα-LBD-GAL4DBD or pSG5- PPARγ LBD-GAL4DBD and pGL4.70 Renilla vectors. Cells were stimulated with gemfibrozil (GEM, 10 μM) and rosiglitazone (ROSI, 100 nM), as positive controls for PPARα and PPARγ, respectively, and compound 2 (10 μM). (B) HepG2 cells were transfected with p(UAS)5XTKLuc, pSG5-LXRα LBD-GAL4DBD or pSG5-LXRβ LBD-GAL4DBD and pGL4.70 Renilla vectors. Cells were stimulated with GW3965 (GW, 10 μM) as positive control and compound 2 (10 μM). (C) HepG2 cells were co-transfected with GPBAR1 and a reporter gene containing a cAMP responsive element in front of the luciferase gene. Cells were stimulated with 2 (50 and 100 μM). TLCA (10 μM) was used as positive control. Luciferase activity served as a measure of the rise in intracellular cAMP following activation of GPBAR1. In all panels, results are expressed as mean ± standard error. ∗p < 0.05 versus not treated cells (NT).