Fig. 5.

Curcumin does not inhibit RICK-induced NF-κB activation. A to C, HEK293T cells were cotransfected with NF-κB-luciferase and β-galactosidase reporter constructs and Nod2 expression vector. Twenty-four hours after transfection, the cells were treated with curcumin (10, 20, and 30 μM) for 6 h (A) or pretreated with curcumin (10 and 20 μM) for 1 h and then coincubated with 200 ng/ml MDP for an additional 6 h (B) or pretreated with parthenolide (5, 10, and 15 μM) for 1 h and then coincubated with 200 ng/ml MDP for additional 6 h (C). D and E, HEK293T cells were cotransfected with RICK expression vector and NF-κB-luciferase and β-galactosidase reporters. Twenty-four hours after transfection, the cells were treated with curcumin (10, 20, and 30 μM) (D) or parthenolide (5, 10, and 15 μM) (E) for 6 h. Cell lysates were prepared and luciferase and β-galactosidase enzyme activities were measured as described under Materials and Methods. RLA was normalized with β-galactosidase activity. Values are mean ± S.E.M (n = 3). Statistical significant difference (p < 0.05) is indicated between cells treated with vehicle and cells treated with curcumin (A) or between cells treated with MDP alone and cells treated with MDP plus curcumin (B) or parthenolide (C). Abbreviations are the same as described in Fig. 1.