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Action Mechanism of Aspirin Draft.
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Aspirin, a non-steroidal anti-inflammatory drug (NSAIDs), is a commonly known blood thinner and anti-inflammatory. It functions by targeting enzymes involved in the signal pathways results in swelling and inflammation. [1] The molecule targets the COX enzyme which produces a conformational change in the chemical structure stopping the production of prostaglandins, which are located at the cite of abrasion and are associated with inflammation[2]. The conformational change is absolute, effecting the cyclooxyrgenase (COX) class of enzymes more specifically COX-1 and COX-2, which are associated with the response to injury and infection.[1] The change observed is irreversible therefore the creation of a new enzyme is necessary before prostaglandins synthesis may resume[3].
Inhibition of Cyclooxyrgenase (COX)
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Aspirin competes for the binding site on the COX enzyme, preventing other signal molecules from attaching and activating the enzyme. Two known COX enzyme subtypes that are known targets of aspirin, are COX-1 and COX-2, both associated with the response to injury and infection. These enzymes influence the production of prostaglandins at the injury site, resulting in swelling and inflammation. Under further investigation have the different functions of COX-1 and COX-1 been uncovered providing key insight to there functions, COX-1 is associated with body regulation and upkeep, where COX-2 is involved with the response to injury and infection.[3] Aspirin is non-selective resulting in the inhibition of both COX enzymes, although the use of selective COX-2 inhibitors, including ibuprofen is a widely studied area. [4]
Aspirin's relationship with prostaglandins (PGs)
[edit]Consequently to the inhibition of the COX enzymes, the signal pathway resulting in prostaglandins (PGs) is blocked, preventing the negative connotations such as fever, pain and inflammation. PG's are chemical signal molecules used by the body as a response to abrasion and infection, the signal molecule then results in the development of five different tissue specific isomerases resulting in the known response to injury and infection. [5]
References
[edit]- ^ a b "How aspirin works". www.uchicagomedicine.org. Retrieved 2023-09-29.
- ^ Ricciotti, Emanuela; FitzGerald, Garret A. (2011-5). "Prostaglandins and Inflammation". Arteriosclerosis, thrombosis, and vascular biology. 31 (5): 986–1000. doi:10.1161/ATVBAHA.110.207449. ISSN 1079-5642. PMC 3081099. PMID 21508345.
{{cite journal}}: Check date values in:|date=(help) - ^ a b Vane, J.R; Botting, R.M (2003-06). "The mechanism of action of aspirin". Thrombosis Research. 110 (5–6): 255–258. doi:10.1016/s0049-3848(03)00379-7. ISSN 0049-3848.
{{cite journal}}: Check date values in:|date=(help) - ^ Zarghi, A.; Arfaei, S.; Ghodsi, R. (2011-06-24). "Design and synthesis of new 2,4,5-triarylimidazole derivatives as selective cyclooxygenase (COX-2) inhibitors". Medicinal Chemistry Research. 21 (8): 1803–1810. doi:10.1007/s00044-011-9710-5. ISSN 1054-2523.
- ^ Ricciotti, Emanuela; FitzGerald, Garret A. (2011-05). "Prostaglandins and Inflammation". Arteriosclerosis, Thrombosis, and Vascular Biology. 31 (5): 986–1000. doi:10.1161/ATVBAHA.110.207449. ISSN 1079-5642. PMC 3081099. PMID 21508345.
{{cite journal}}: Check date values in:|date=(help)CS1 maint: PMC format (link)
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