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. Author manuscript; available in PMC: 2012 Feb 20.
Published in final edited form as: Mol Cell Endocrinol. 2010 Dec 30;333(2):160–171. doi: 10.1016/j.mce.2010.12.028

Figure 9. de novo synthesis of GSH played a pivotal role for curcumin to inhibit the hyperglycemia-induced gene expression of GLUT2 in activated HSCs in vitro.

Figure 9

Passaged HSCs were stimulated with glucose at 450 mg/dl and divided into two groups. One was treated with or without curcumin (20 μM), or NAC (5 mM), for 24 hr. The other group was pretreated with BSO (0.25 mM) for 1 hr prior to the treatment with curcumin (20 μM), or NAC (5 mM), for additional 24 hr. (A). Luciferase activity assays of cells transfected with pGluT2-Luc. The inset denoted the pGluT2-Luc construct in use and the application of curcumin or NAC to the system. *p<0.05 vs cells stimulated with glucose at 450 mg/dl alone. ‡p<0.05 vs cells treated with glucose plus curcumin or NAC. (B). Western blotting analyses of the abundance of GLUT2. Representatives were shown from three independent experiments. Italic numbers were fold changes (means ± S. D) in densities of the bands compared with the control with no treatment (the 1st lane) after normalization (n=3).