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. Author manuscript; available in PMC: 2011 Jun 1.
Published in final edited form as: Gastroenterology. 2010 Mar 12;138(7):2509–2518.e1. doi: 10.1053/j.gastro.2010.03.008

Figure 5. Effects of ROS inhibitor on NF-κB signaling pathway.

Figure 5

An NFκB promoter construct expressing firefly (pNFκB-Luc) and the control construct pRL-TK expressing Renilla luciferase were transfected into cells for 24 hours. The transfected Huh7.5.1 cells or JFH1 cells were incubated with 20 μM different inhibitors for 14 hours. The inhibitors used included DPI, SB, SP, AQ, U0126, or LY. 1% DMSO was used as a negative control. Designations are the same in Figure 5A and B.

Figure 5A. DPI blocks HCV-activated NFκB signaling. Relative luciferase activity (RLA) was normalized by dividing the firefly luciferase value by the Renilla luciferase value. HCV increased NFκB promoter signaling by over two fold. DPI and AQ completely blocked NFκB signaling. SB, SP, and U0126 reduced NFκB signaling by 82.9%, 76.7%, and 52.1%, respectively. In contrast, LY 294002 had no effect on NFκB signaling.

Figure 5B. DPI blocked HCV-mediated NFκB phosphorylation. HCV activated NFκB phosphorylation in JFH1 cells compared to Huh7.5.1 cells. DPI and AQ blocked NFκB phosphorylation. SB, SP, or U0126 partially reduced NFκB phosphorylation. In contrast, LY had no effect on NFκB phosphorylation. Lane#1 Huh7.5.1, #2 JFH1, Lane#3 JFH1+DPI; Lane#4 JFH1+SB; #5 JFH1+SP; #6 JFH1+AQ; #7 JFH1+U0126; #8 JFH1+LY.