Figure 4.

Curcumin inhibited PKA activity, which facilitated the increase in the activity of GK and the reduction in intracellular glucose in cultured HSCs. (A) Serum-starved HSCs were pretreated with curcumin at indicated concentrations for 1 h prior to the stimulation with or without leptin (100 ng·mL⁻¹) in serum-free media for additional 30 min. Levels of p-PKA were evaluated by Western blotting analyses. Total PKA was used as an invariant control for equal loading. Representative blots are presented from three independent experiments. Italic numbers beneath blots were fold changes in the densities of the bands compared to the control without treatment in the blot (n = 3), after normalization with the internal invariable control. (B,C) Serum-starved HSCs were pretreated with the PKA inhibitor H89 at indicated concentrations, or with curcumin (20 µM), in serum-free media for 1 h prior to the addition of leptin (100 ng·mL⁻¹) for additional 30 min. *P < 0.05 versus the untreated control (the second column). (B) Analyses of GK activities. Values were expressed as fold changes compared with the untreated control (means ± SD) (n = 3). (C) Determination of levels of intracellular glucose. Values were expressed as pmol glucose·µg⁻¹ protein (means ± SD) (n = 3).