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Chunk #31 — 2. Inhibitors of the NF-κB activation pathway — 2.8. Other mechanisms of NF-κB inhibition — 2.8.4. Anti-inflammatory and immunosuppressive agents

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Inhibiting NF-κB activation by small molecules as a therapeutic strategy.
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NSAIDs such as sodium salicylate (aspirin) and sulindac have been reported to inhibit NF-κB activation by inhibiting IκBα phosphorylation [170, 171]. At higher concentrations, aspirin has been shown to block NF-κB activity by directly binding to and inhibiting the kinase activity of IKKβ by reducing its ability to bind ATP [172]. More recently, aspirin was reported to inhibit proteasome activity [173]. As such, high-dose aspirin therapy may have applications in treating diseases in which NF-κB activity is involved, including cancer [174], diabetes [175], and heart disease [176]. Other NSAIDs such as ibuprofen and indomethacin have also been reported to inhibit NF-κB activation in cell culture [177–180].