(A) and (B): Semi-confluent HSCs were co-transfected with the plasmid pLOX-1-Luc and the plasmid pPPARγ (A), or its mutant counterpart pdn-PPARγ (B), at indicated doses. After recovery, cells were treated with or without curcumin (20μM) for 24 hr. Luciferase activities were expressed as relative units after β-galactosidase normalization (means ± s.d.; n≥6). *P<0.05 versus cells without pPPARγ, or pdn-PPARγ, (the first column on the left). ‡P<0.05 versus cells transfected with no pdn-PPARγ and treated with curcumin only (the second column). The floating schema denoted pLOX-1-Luc in use and co-transfected plasmid pPPARγ or pdn-PPARγ ± curcumin in the system. (C) and (D): Serum-starved HSCs were treated with the natural PPARγ agonist PGJ2 at 0-15μM for 24 hr. (C). Real-time PCR assays of LOX-1 mRNA. mRNA fold changes were expressed as means ± s.d. (n≥3). *P<0.05 versus the untreated control (the first column on the left); (D). Western blotting analyses of LOX-1. β-actin was used as an internal control for equal protein loading. Representative was from three independent experiments. Italic numbers beneath the blot were fold changes in the densities of the bands compared to the control without treatment in the blot (n=3), after normalization with β-actin. Because of the limited space, standard deviations were not presented.