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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 469))

Abstract

Cyclooxygenase (Cox) is a ubiquitous enzyme involved in various inflammatory processes. Two isoforms of Cox have been identified, Cox-1 and Cox-2. Cox-1 is constitutively expressed in most tissues and mediates physiologic responses such as regulation of renal sodium and water reabsorption, vascular homeostasis, and cytoprotection of the stomach. By comparison Cox-2 is primarily considered an inducible immediate-early gene whose synthesis can be upregulated by mitogenic or inflammatory stimuli including: tumor promoters 1, IL-1β 2, endotoxins 3, growth factors 4, and serum5. The pathophysiological role of Cox has been the topic of much interest. Cox is the main therapeutic target for non-steroidal anti-inflammatory drugs (NSAIDs) which exhibit their antipyretic, analgesic, and anti-inflammatory effects in humans via inhibition of prostaglandin biosynthesis 6. NSAIDS have been effective in the reduction of inflammatory symptoms in carrageenan-induced rat paw inflammation models 7 and in the reduced incidence of colon cancer 8,9.

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© 1999 Springer Science+Business Media New York

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Guan, Z., Buckman, S.Y., Springer, L.D., Morrison, A.R. (1999). Regulation of Cyclooxygenase-2 by the Activated p38 Mapk Signaling Pathway. In: Honn, K.V., Marnett, L.J., Nigam, S., Dennis, E.A. (eds) Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation, and Radiation Injury, 4. Advances in Experimental Medicine and Biology, vol 469. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4793-8_2

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  • DOI: https://doi.org/10.1007/978-1-4615-4793-8_2

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-7171-7

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