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

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,...

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Bibliographic Details
Main Authors: M. Castro-caldas (Author), A. F. Mendes (Author), A. P. Carvalho (Author), C. B. Duarte (Author), M. C. Lopes (Author)
Format: Book
Published: Hindawi Limited, 2003-01-01T00:00:00Z.
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Summary: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.
Item Description:0962-9351
1466-1861
10.1080/0962935031000096953