Figure 6

The interruption of PI-3K/AKT, JNK or ERK signaling alters the expression of proteins relevant to cell cycle and apoptosis in activated HSC. Serum-starved HSC were divided into two groups. One group was treated with curcumin (20 μM), or one of the kinase inhibitors at the indicated concentrations, in DMEM with FBS (10%) for 24 h. The other group was pretreated with PD68235, a specific PPARγ inhibitor, at 20 μM for 30 min before the addition of curcumin (20 μM), or one of the inhibitors at the indicated concentrations in the media with FBS (10%) for an additional 24 h. Whole-cell extracts were prepared for Western blotting analyses. The levels of the cell cycle-stimulating protein Cyclin D1, the antiapoptotic protein Bcl-2 and the proapoptotic protein Bax were, respectively, detected. Representatives from three independent experiments were shown. (a) Cells were treated with LY294002 with or without the PPARγ antagonist PD68235; (b) Cells were treated with PD98059 with or without the PPARγ antagonist PD68235; (c) Cells were treated with SP600125 with or without the PPARγ antagonist PD68235.