Figure 1
Figure 1. PMA-stimulated superoxide release by U937 cells. Wild-type U937 cells (A) and U937 cells transfected with empty vector (B) show that the NF-κB inhibitors dexamethasone and gliotoxin inhibited superoxide release by myelomonocytic cells induced to differentiate by IFN-γ and TNF-α (*P < .05 in all situations; n = 8, Mann-Whitney test). (C) Complete suppression of superoxide generation in a U937 subclone transfected with IκB S32A/S36A, including cells not exposed to any exogenous inhibitor (lane 2). In all panels: lanes 1, 3, and 5, undifferentiated U937 cells; lanes 2, 4, and 6, U937 cells induced to differentiate by IFN-γ and TNF-α; lanes 1 and 2, no inhibitor; lanes 3 and 4, dexamethasone (1 μmol/L); lanes 5 and 6, gliotoxin (10 μmol/L).

PMA-stimulated superoxide release by U937 cells. Wild-type U937 cells (A) and U937 cells transfected with empty vector (B) show that the NF-κB inhibitors dexamethasone and gliotoxin inhibited superoxide release by myelomonocytic cells induced to differentiate by IFN-γ and TNF-α (*P < .05 in all situations; n = 8, Mann-Whitney test). (C) Complete suppression of superoxide generation in a U937 subclone transfected with IκB S32A/S36A, including cells not exposed to any exogenous inhibitor (lane 2). In all panels: lanes 1, 3, and 5, undifferentiated U937 cells; lanes 2, 4, and 6, U937 cells induced to differentiate by IFN-γ and TNF-α; lanes 1 and 2, no inhibitor; lanes 3 and 4, dexamethasone (1 μmol/L); lanes 5 and 6, gliotoxin (10 μmol/L).

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