Dexamethasone prevents interleukin-1β-induced nuclear factor-κB activation by upregulating IκB-α synthesis, in lymphoblastic cells

Abstract

Aims: Glucocorticoids (GCs) exert some of their anti-inflammatory actions by preventing the activation of the transcription factor nuclear factor (NF)-κB. The GC-dependent inhibition of NF-κB may occur at different levels, but the mechanisms involved are still incompletely understood. In this work, we investigated whether the synthetic GC, dexamethasone (Dex), modulates the activity of NF-κB in the lymphoblastic CCRF-CEM cell line. We also evaluated the ability of Dex to prevent the activation of NF-κB in response to the potent proinflammatory cytokine, interleukin (IL)-1β.

Keywords

• Nuclear factor-κB
• Dexamethasone
• IκB-α
• Interleukin-1β
• Lymphoblastic cells.