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. 2017 Apr 24;292(24):10275–10287. doi: 10.1074/jbc.M116.770974

Figure 1.

Figure 1.

Up-regulation of hepcidin expression by IL-1β in hepatocytes. Primary mouse and rat hepatocytes (A and B) were treated with IL-1β (25 ng/ml) for 24 h. The expression of hepcidin (A) and iNOS (B) was examined by RT-qPCR analysis with the levels in the control cells defined as 1. The data are presented as the mean ± S.E. (n = 4). **, p < 0.01 versus cells treated without IL-1β. C, HepG2 cells were treated with IL-1β (25 ng/ml) for the indicated time. The expression of hepcidin was examined by RT-qPCR analysis with the levels in the control cells prior to IL-1β treatment defined as 1. The data are presented as the mean ± S.E. (n = 3). **, p < 0.01 versus cells treated without IL-1β at the respective time point. D and E, HepG2 cells were either untreated or pretreated with BAY 11-7085 (5 μm, BAY: D) or cycloheximide (1 μg/ml, CHX, E) before treatment with IL-1β (10 or 25 ng/ml) for 12 h. Hepcidin expression was examined by RT-qPCR analysis. The expression levels in control cells treated without either BAY 11-7085 or cycloheximide were defined as 1. The data are presented as the mean ± S.E. (n = 3). *, p < 0.05 and **, p < 0.01 versus cells treated with the respective inhibitor (vehicle, BAY 11-7085, or cycloheximide) in the absence of IL-1β. †, p < 0.05 and ††, p < 0.01 versus cells with corresponding IL-1β treatments in the absence of inhibitor (i.e. BAY 11-7085 (D) or cycloheximide (E)).