Abstract
Prostanoids play pivotal roles in inflammation and pain. Cyclooxygenase (COX) inhibitors, the nonsteroidal anti-inflammatory drugs (NSAIDs), depress prostanoid formation and are widely used to treat inflammatory pain. However, their therapeutic benefit is offset by serious side-effects, primarily gastrointestinal and cardiovascular complications. Pathway elements downstream of the COX enzymes, particularly the terminal synthases and receptors of prostaglandin E2, have been proposed as alternative targets for the development of novel NSAID like drugs. Here, we summarize the current knowledge on the roles of individual prostanoids in modulating inflammatory pain.
Copyright © 2012 Elsevier Inc. All rights reserved.
MeSH terms
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Anti-Inflammatory Agents, Non-Steroidal / pharmacology
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Cyclooxygenase 2 / metabolism*
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Cyclooxygenase Inhibitors / pharmacology
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Humans
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Inflammation / drug therapy
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Inflammation / metabolism
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Inflammation / physiopathology
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Intramolecular Oxidoreductases / antagonists & inhibitors
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Intramolecular Oxidoreductases / metabolism*
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Pain / drug therapy
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Pain / metabolism*
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Pain / physiopathology
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Prostaglandin-E Synthases
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Prostaglandin-Endoperoxide Synthases / metabolism
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Prostaglandins / metabolism*
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Receptors, Prostaglandin E, EP2 Subtype / antagonists & inhibitors
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Receptors, Prostaglandin E, EP2 Subtype / metabolism
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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Cyclooxygenase Inhibitors
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Prostaglandins
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Receptors, Prostaglandin E, EP2 Subtype
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Cyclooxygenase 2
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PTGS2 protein, human
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Prostaglandin-Endoperoxide Synthases
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Intramolecular Oxidoreductases
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Prostaglandin-E Synthases