Research Article

Chloroquine and Rapamycin Augment Interleukin-37 Expression via the LC3, ERK, and AP-1 Axis in the Presence of Lipopolysaccharides

Figure 5

Cell signaling pathways contributing to the inductive transcription of IL-37. (a) The effect of LPS and autophagy-modifying reagents on the contents of phosphorylated NF-κB p65/IκBα and phosphorylated AP-1 (c-Fos/c-Jun) proteins. Two independent experiments were repeated and yielded similar results. The representative western blot images were shown. (b) The effect of MAPK inhibitors and NF-κB inhibitor on the expression of IL-37 and IL-1β induced by LPS and rapamycin treatment in U937 cells. Each sample was assayed in triplicate, and the results were shown in Inhibitors used in this study included SB 203580 (100 μM), U0126 (200 μM), SP600125 (20 μM), and BAY 11-7082 (10 μM). S.S.U.B: combination of the four inhibitors. (c) The effect of MAPK agonists on IL-37, IL-1β, and IL-18 expression in untreated U937 macrophages was also investigated. The agonists were LM22B-10 at 125, 250, 500, and 1000 nM and anisomycin at 1.25, 2.5, 5, and 10 μM. Each sample was assayed in triplicate (). (d) The effect of LPS and autophagy-modifying reagents on the contents of phosphorylated Erk1/2 and phosphorylated p38 MAPK. Two independent experiments were repeated and yielded similar results. The representative western blot images were shown.
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