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. Author manuscript; available in PMC: 2014 Nov 1.
Published in final edited form as: Lab Invest. 2014 Mar 10;94(5):503–516. doi: 10.1038/labinvest.2014.42

Figure 10. The inhibition of the activity of GCL by BSO abolished the role of NAC and curcumin, and mimicked the effects of AGEs on the divergent regulation of gene expression of RAGE and AGE-R1 in HSC.

Figure 10

Serum-starved HSC were divided into two groups. In one group, cells were stimulated with AGEs (100 μg/ml), or AGEs plus curcumin (Cur) (20 μM), or NAC (5 mM), in serum-depleted media for 24 h. Control cells received no treatment. In the other group, cells were pretreated with BSO (0.25 mM) for 1 h before the addition of AGEs (100 μg/ml), or AGEs plus curcumin (20 μM), or NAC (5 mM), in serum-free media for additional 24 h. Total RNA or whole cell extracts were prepared. A, Real-time PCR analyses of RAGE and AGE-R1 mRNA. Values were expressed as mRNA fold changes (means ± SD) (n= 3). *P<0.05 vs. the untreated control (the corresponding 1st column); ‡P<0.05 vs. cells treated with AGEs only (the corresponding 2nd column); §P<0.05, vs. cells treated with AGEs plus curcumin, or NAC, (the corresponding 3rd or 4th column, respectively). B, Western blotting analyses of RAGE and AGE-R1. β-actin was used as an invariant control for equal loading. Representatives were presented from three independent experiments.