Figure 3.

CAB inhibited PPARγ transcriptional activity as evaluated by transactivation assay. HEK293T cells were co-transfected with PPARγ, RXRα and reporter gene, while the control plasmids were treated (A) with or (B) without rosiglitazone (2.5 μmol/L) and increasing concentrations of CAB for 18 h. The cells were harvested for luciferase and β-galactosidase assays. The luciferase activity was normalized with β-galactosidase activity. The concentration of GW9662 (PPARγ antagonist) was 1 μmol/L.