Ibuprofen
From Proteopedia
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Like aspirin and indomethacin, ibuprofen is a nonselective COX inhibitor, in that it inhibits two isoforms of cyclooxygenase, COX-1 and COX-2. The analgesic, antipyretic, and anti-inflammatory activity of NSAIDs appears to operate mainly through inhibition of COX-2, which decreases the synthesis of prostaglandins involved in mediating inflammation, pain, fever, and swelling. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation. Inhibition of COX-1 instead would be responsible for unwanted effects on the gastrointestinal tract.<ref name="R53">PMID:19203472</ref> 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.<ref name="R54">PMID:18363350</ref> | Like aspirin and indomethacin, ibuprofen is a nonselective COX inhibitor, in that it inhibits two isoforms of cyclooxygenase, COX-1 and COX-2. The analgesic, antipyretic, and anti-inflammatory activity of NSAIDs appears to operate mainly through inhibition of COX-2, which decreases the synthesis of prostaglandins involved in mediating inflammation, pain, fever, and swelling. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation. Inhibition of COX-1 instead would be responsible for unwanted effects on the gastrointestinal tract.<ref name="R53">PMID:19203472</ref> 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.<ref name="R54">PMID:18363350</ref> | ||
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| + | Unlike most other NSAIDs, ibuprofen also acts as an inhibitor of Rho kinase and may be useful in recovery from spinal-cord injury.<ref name="R56">PMID:22350947</ref><ref name="R57">PMID:33197553</ref> | ||
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== References == | == References == | ||
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Revision as of 12:32, 26 June 2023
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References
- ↑ Rao P, Knaus EE. Evolution of nonsteroidal anti-inflammatory drugs (NSAIDs): cyclooxygenase (COX) inhibition and beyond. J Pharm Pharm Sci. 2008 Sep 20;11(2):81s-110s. PMID:19203472 doi:10.18433/j3t886
- ↑ Kakuta H, Zheng X, Oda H, Harada S, Sugimoto Y, Sasaki K, Tai A. Cyclooxygenase-1-selective inhibitors are attractive candidates for analgesics that do not cause gastric damage. design and in vitro/in vivo evaluation of a benzamide-type cyclooxygenase-1 selective inhibitor. J Med Chem. 2008 Apr 24;51(8):2400-11. PMID:18363350 doi:10.1021/jm701191z
- ↑ Kopp MA, Liebscher T, Niedeggen A, Laufer S, Brommer B, Jungehulsing GJ, Strittmatter SM, Dirnagl U, Schwab JM. Small-molecule-induced Rho-inhibition: NSAIDs after spinal cord injury. Cell Tissue Res. 2012 Jul;349(1):119-32. PMID:22350947 doi:10.1007/s00441-012-1334-7
- ↑ Luo M, Li YQ, Lu YF, Wu Y, Liu R, Zheng YR, Yin M. Exploring the potential of RhoA inhibitors to improve exercise-recoverable spinal cord injury: A systematic review and meta-analysis. J Chem Neuroanat. 2021 Jan;111:101879. PMID:33197553 doi:10.1016/j.jchemneu.2020.101879
