Non-steroidal anti-inflammatory drugs such as ibuprofen work by inhibiting the enzyme cyclooxygenase (COX), which converts arachidonic acid to prostaglandin H2 (PGH2). PGH2, in turn, is converted by other enzymes to several other prostaglandins (which are mediators of pain, inflammation, and fever) and to thromboxane A2 (which stimulates platelet aggregation, leading to the formation of blood clots).
Like aspirin, indomethacin, and most other NSAIDs, ibuprofen is considered a non-selective COX inhibitor—that is, it inhibits two isoforms of cyclooxygenase, ''COX-1'' and ''COX-2''. The analgesic, antipyretic, and anti-inflammatory activity of NSAIDs appears to be achieved mainly through inhibition of COX-2, whereas inhibition of COX-1 would be responsible for unwanted effects on platelet aggregation and the gastrointestinal tract. However, the role of the individual COX isoforms in the analgesic, anti-inflammatory, and gastric damage effects of NSAIDs is uncertain and different compounds cause different degrees of analgesia and gastric damage.
Further Reading
This article is licensed under the Creative Commons Attribution-ShareAlike License.
It uses material from the Wikipedia article on
"Ibuprofen"
All material adapted used from Wikipedia is available under the terms of the
Creative Commons Attribution-ShareAlike License.
Wikipedia® itself is a registered trademark of the Wikimedia Foundation, Inc.