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Titlebook: Improved Non-Steroid Anti-Inflammatory Drugs: COX-2 Enzyme Inhibitors; John Vane,Jack Botting,Regina Botting Book 1996 Kluwer Academic Pub

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发表于 2025-3-21 18:21:49 | 显示全部楼层 |阅读模式
书目名称Improved Non-Steroid Anti-Inflammatory Drugs: COX-2 Enzyme Inhibitors
编辑John Vane,Jack Botting,Regina Botting
视频video
图书封面Titlebook: Improved Non-Steroid Anti-Inflammatory Drugs: COX-2 Enzyme Inhibitors;  John Vane,Jack Botting,Regina Botting Book 1996 Kluwer Academic Pub
描述In 1971, Vane proposed that the mechanism of action of the aspirin-like drugs was through their inhibition of prostaglandin biosynthesis. Since then, there has been intense interest in the interaction between this diverse group of inhibitors and the enzyme known as cyclooxygenase (COX). It exists in two isoforms, COX-l and COX-2 (discovered some 5 years ago). Over the last two decades several new drugs have reached the market based on COX-l enzyme screens. Elucidation of the three-dimensional structure of COX-l has provided a new understanding for the actions of COX inhibitors. The constitutive isoform of COX, COX-l has clear physiological functions. Its activation leads, for instance, to the production of prostacyclin which when released by the endothelium is anti-thrombogenic and anti-atherosclerotic, and in the gastric mucosa is cyto­ protective. COX-l also generates prostaglandins in the kidney, where they help to maintain blood flow and promote natriuresis. The inducible isoform, COX-2, was discovered through its activity being increased in a number of cells by pro­ inflammatory stimuli. A year or so later, COX-2 was identified as a distinct isoform encoded by a different gene
出版日期Book 1996
关键词cardiovascular disease; inflammation; kidney; kinetics; pharmacokinetics; pharmacology; research; toxicity
版次1
doihttps://doi.org/10.1007/978-94-010-9029-2
isbn_softcover978-94-010-9031-5
isbn_ebook978-94-010-9029-2
copyrightKluwer Academic Publishers and William Harvey Press 1996
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COX-2 expression and inhibition in human monocytes,isoform found in gastrointestinal tissue.. Prostanoid production by COX-1 is involved in physiological functions such as vascular homeostasis, control of kidney function and gastric cytoprotection.. COX-2 is induced in a more restricted, cell-specific fashion by mitogenic and inflammatory stimuli..
发表于 2025-3-22 06:10:07 | 显示全部楼层
Expression and regulation of COX-2 in synovial tissues of arthritic patients,th factors and eicosanoids, produced by infiltrating mononuclear cells as well as by endothelial cells and fibroblast-like cells (synoviocytes), contribute to the proliferative and invasive phenotype of inflamed synovial tissues in RA.
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The three-dimensional structure of cyclooxygenases, and indomethacin.. NSAIDs have been the common way to treat certain symptoms of inflammatory. and cardiovascular diseases.. Moreover, a role for aspirin as an anticancer prophylaxis is now quite established. although the precise molecular basis for this effect is still unclear.
发表于 2025-3-22 19:30:53 | 显示全部楼层
The dilemma of two cyclooxygenases: identifying the roles of COX-1 and COX-2 in inflammation and ap induced by agents that cause the cells in question to differentiate, reinforcing the notion that the role of COX-1 is in the maintenance of differentiated homeostasis.. In these cases, COX-1 induction is long-term or permanent.
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Re-evaluation of gut toxicity of NSAIDs, particular pharmaceutical preparation on the gut lining, the extent and variability of first-pass metabolism of the parent compound in the gut wall and liver, the effect of disease states or age on clearance and the potential biological activity of metabolites.
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Differential inhibition of COX-1 and COX-2 in vitro and pharmacological profile in vivo of NSAIDs,h cyclooxygenase blockade is the mechanism of action of aspirin and related NSAIDs, it has been widely accepted that the mechanisms underlying both the therapeutic (i.e. anti-inflammatory) actions and the side effects of NSAIDs on the gastric mucosa, renal function and platelet aggregation are closely related.
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