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0026-895X/97/030421-09$3.00/0
Copyright © by The American Society for Pharmacology and Experimental Therapeutics
All rights of reproduction in any form reserved.
MOLECULAR PHARMACOLOGY 52:421-429 (1997).

Aspirin Inhibits Tumor Necrosis Factor-alpha Gene Expression in Murine Tissue Macrophages

Rodney E. Shackelford, Paul B. Alford, Yan Xue, Sheau-Fung Thai, Dolph O. Adams, and Salvatore Pizzo

Department of Pathology, Duke University Medical Center, Durham, North Carolina 27710

Aspirin has been reported to inhibit the activation of nuclear factor-kappa B (NF-kappa B) through stabilization of inhibitor kappa B (Ikappa B). This observation led us to investigate the role of aspirin in suppressing the activation of the NF-kappa B-regulated tumor necrosis factor-alpha (TNF-alpha ) gene expression in primary macrophages. We now report that therapeutic doses of aspirin suppress lipopolysaccharide-inducible NF-kappa B binding to an NF-kappa B binding site in the TNF-alpha promoter, lipopolysaccharide-induced TNF-alpha mRNA accumulation, and protein secretion. Ikappa B is also stabilized under these conditions. The aspirin-initiated stabilization of Ikappa B, suppression of induced TNF-alpha mRNA, and NF-kappa B binding to the TNF-alpha promoter are blocked by pretreatment with pertussis toxin. These studies suggest that aspirin may exert significant anti-inflammatory effects by suppressing the production of macrophage-derived inflammatory mediators.

Copyright © by The American Society for Pharmacology and Experimental Therapeutics


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