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.
Mesh Terms:
Animals, Aspirin, Cell Line, Enhancer Elements, Genetic, Gene Expression, Genes, Reporter, HIV Long Terminal Repeat, HIV-1, Humans, Immunoglobulin kappa-Chains, Lipopolysaccharides, Mice, NF-kappa B, Phosphorylation, Promoter Regions, Genetic, Protein Biosynthesis, Proto-Oncogene Proteins, Sodium Salicylate, T-Lymphocytes, Transcription Factor RelB, Transcription Factors, Transfection, Tumor Cells, Cultured
Animals, Aspirin, Cell Line, Enhancer Elements, Genetic, Gene Expression, Genes, Reporter, HIV Long Terminal Repeat, HIV-1, Humans, Immunoglobulin kappa-Chains, Lipopolysaccharides, Mice, NF-kappa B, Phosphorylation, Promoter Regions, Genetic, Protein Biosynthesis, Proto-Oncogene Proteins, Sodium Salicylate, T-Lymphocytes, Transcription Factor RelB, Transcription Factors, Transfection, Tumor Cells, Cultured
Science
Date: Aug. 12, 1994
PubMed ID: 8052854
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