Skip to main content
. 2015 Jan 27;10(1):e0116773. doi: 10.1371/journal.pone.0116773

Fig 3. Effects of IKK2 and MAPK inhibitors on repression of dexamethasone-induced 2×GRE reporter activation by TNF.

Fig 3

A. BEAS-2B cells stably transfected with a 2×glucocorticoid response element (GRE) luciferase reporter were pre-treated for 30 min with 10 μM of the NF-κB or MAPK pathway inhibitors: PS-1145 (PS; IKBKB), PD098059 (PD; MAP2K1/2), SB203580 (SB; p38 MAPKs) or JNK inhibitor VIII (JNK; JNK MAPKs), before addition of 10 ng/ml of tumor necrosis factor-α (TNF). After 1 h, 10 μM dexamethasone (Dex) was added and cells harvested 6 h later for luciferase assay. Data (n = 7), expressed as a percentage of Dex activation, are plotted as means ± S.E. BEAS-2B 2×GRE cells were pre-treated for 30 min with the indicated concentrations of B. PS or JNK or C. JNK in the presence or absence of 10 μM PS, before addition of 10 ng/ml TNF. After 1 h, 10 μM Dex was added and cells harvested 6 h later for luciferase assay. Data (n = 4–8), expressed as fold activation, are plotted as means ± S.E. Significance was tested using repeated measures, one-way analysis of variance (ANOVA) with Bonferroni’s correction for multiple comparisons. *, P<0.05; **, P<0.01; ***, P<0.001. D+T indicates Dex plus TNF treatment.