Abstract
Two, non-prostaglandin effects of antiinflammatory levels of salicylates (i.e.aspirin III) are shown here: 1) Exposure of neutrophils to aspirin or sodium salicylate inhibited Erk activity and integrin-dependent aggregation of neutrophils, consistent with anti-inflammation but not COX inhibition. Inhibition of Mek (proximal activator of Erk) also blocked stimulation of Erk and neutrophil aggregation by FMLP and arachidonic acid. Thus, the antiinflammatory effects of salicylates may be mediated by inhibition of Erk signaling required for integrin-mediated responses. 2) Acute inflammation was induced in murine air-pouches of wild-type mice and mice rendered deficient in either COX-2 or pl 05, the precursor of p50 of NFiB. The antiinflammatory effects of aspirin and sodium salicylate were independent of the presence of COX-2 or p105 component of NFKB or the levels of prostaglandins at the inflammatory site. In contrast, glucocorticoid action depended on the p105.
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Weissmann, G., Montesinos, M.C., Pillinger, M., Cronstein, B.N. (2002). Non-Prostaglandin Effects of Aspirin III and Salicylate: Inhibition of Integrin-dependent Human Neutrophil Aggregation and Inflammation in COX 2- and NFκB (P105)-Knockout Mice. In: Honn, K.V., Marnett, L.J., Nigam, S., Dennis, E., Serhan, C. (eds) Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury, 5. Advances in Experimental Medicine and Biology, vol 507. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0193-0_87
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DOI: https://doi.org/10.1007/978-1-4615-0193-0_87
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