COX enzyme: Difference between revisions
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COX or cyclo-oxygenase enzymes produce prostaglandins | COX or cyclo-oxygenase enzymes produce prostaglandins which promote [[Inflammation|inflammatory]] actions such as pain, inflammation and fever essential for the mechanisms involved in healing and recovery<ref>Omudhome Ogbru P. NSAIDs: Drug List, Names, and Side Effects [Internet]. MedicineNet. 2017 [cited 1 December 2017]. Available from: https://www.medicinenet.com/nonsteroidal_antiinflammatory_drugs/article.htm</ref>. There are two COX enzymes, [[COX-1|COX-1]] and [[COX-2|COX-2]]. They can be inhibited by [[Non-steroidal anti-inflammatory drugs|non-steroidal anti-inflammatory drugs]] (NSAIDS) such as ibuprofen, paracetamol and mefenamic acid. The analgesic action of nonsteroidal anti-inflammatory drugs (NSAIDs) has been explained on the basis of their inhibition of these enzymes, COX-1 and COX-2, that synthesize [[prostaglandins|prostaglandins]]. | ||
*COX-1 is a constitutive member of normal cells and COX-2 is induced in inflammatory cells. | *COX-1 is a constitutive member of normal cells and COX-2 is induced in inflammatory cells. | ||
*Inhibition of COX-2 activity | *Inhibition of COX-2 activity represents the most likely mechanism of action for [[Non-steroidal anti-inflammatory drugs|NSAID]]-mediated analgesia, while the ratio of inhibition of COX-1 to COX-2 by NSAIDs should determine the likelihood of adverse effects. In addition, some NSAIDs inhibit the lipoxygenase pathway, which may itself result in the production of algogenic [[Metabolites|metabolites]]. Interference with[[G-protein|G-protein]]-mediated signal transduction by [[Non-steroidal anti-inflammatory drugs|NSAIDs]] may form the basis of an [[Analgesic|analgesic mechanism]] unrelated to inhibition of prostaglandin synthesis<ref>Cashman J. The Mechanisms of Action of NSAIDs in Analgesia. Drugs [Internet]. 1996 [cited 3 December 2017];52(Supplement 5):13-23. Available from: https://www.ncbi.nlm.nih.gov/pubmed/8922554</ref>. | ||
=== References === | === References === | ||
<references /> | <references /> | ||
Latest revision as of 19:51, 4 December 2017
COX or cyclo-oxygenase enzymes produce prostaglandins which promote inflammatory actions such as pain, inflammation and fever essential for the mechanisms involved in healing and recovery[1]. There are two COX enzymes, COX-1 and COX-2. They can be inhibited by non-steroidal anti-inflammatory drugs (NSAIDS) such as ibuprofen, paracetamol and mefenamic acid. The analgesic action of nonsteroidal anti-inflammatory drugs (NSAIDs) has been explained on the basis of their inhibition of these enzymes, COX-1 and COX-2, that synthesize prostaglandins.
- COX-1 is a constitutive member of normal cells and COX-2 is induced in inflammatory cells.
- Inhibition of COX-2 activity represents the most likely mechanism of action for NSAID-mediated analgesia, while the ratio of inhibition of COX-1 to COX-2 by NSAIDs should determine the likelihood of adverse effects. In addition, some NSAIDs inhibit the lipoxygenase pathway, which may itself result in the production of algogenic metabolites. Interference withG-protein-mediated signal transduction by NSAIDs may form the basis of an analgesic mechanism unrelated to inhibition of prostaglandin synthesis[2].
References
- ↑ Omudhome Ogbru P. NSAIDs: Drug List, Names, and Side Effects [Internet]. MedicineNet. 2017 [cited 1 December 2017]. Available from: https://www.medicinenet.com/nonsteroidal_antiinflammatory_drugs/article.htm
- ↑ Cashman J. The Mechanisms of Action of NSAIDs in Analgesia. Drugs [Internet]. 1996 [cited 3 December 2017];52(Supplement 5):13-23. Available from: https://www.ncbi.nlm.nih.gov/pubmed/8922554