Inhibition of NF-kappa B by sodium salicylate and aspirin.
The transcription factor nuclear factor-kappa B (NF-kappa B) is critical for the inducible expression of multiple cellular and viral genes involved in inflammation and infection including interleukin-1 (IL-1), IL-6, and adhesion molecules. The anti-inflammatory drugs sodium salicylate and aspirin inhibited the activation of NF-kappa B, which further explains the mechanism of action of these drugs. This inhibition prevented the degradation of the NF-kappa B inhibitor, I kappa B, and therefore NF-kappa B was retained in the cytosol. Sodium salicylate and aspirin also inhibited NF-kappa B-dependent transcription from the Ig kappa enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells.
Kopp
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Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06536.
Ghosh
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S
D000818:Animals; D001241:Aspirin / Q000494:pharmacology*; D002460:Cell Line; D004742:Enhancer Elements, Genetic; D015870:Gene Expression / Q000187:drug effects; D017930:Genes, Reporter; D016325:HIV Long Terminal Repeat; D015497:HIV-1 / Q000235:genetics; D006801:Humans; D007145:Immunoglobulin kappa-Chains / Q000235:genetics; D008070:Lipopolysaccharides / Q000494:pharmacology; D051379:Mice; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000378:metabolism; D010766:Phosphorylation; D011401:Promoter Regions, Genetic; D014176:Protein Biosynthesis / Q000187:drug effects; D011518:Proto-Oncogene Proteins / Q000378:metabolism; D012980:Sodium Salicylate / Q000494:pharmacology*; D013601:T-Lymphocytes / Q000378:metabolism; D051841:Transcription Factor RelB; D014157:Transcription Factors; D014162:Transfection; D014407:Tumor Cells, Cultured
D007145:Immunoglobulin kappa-Chains; D008070:Lipopolysaccharides; D016328:NF-kappa B; D011518:Proto-Oncogene Proteins; C497593:RELB protein, human; C497594:Relb protein, mouse; D014157:Transcription Factors; D051841:Transcription Factor RelB; D001241:Aspirin; D012980:Sodium Salicylate