Hvad er virkningsmekanismen for aspirin?
Mechanism of action of aspirin
Aspirin har flere forskellige virkninger i kroppen, primært reduktion af inflammation, analgesi (smertelindring), forebyggelse af blodpropper og reduktion af feber. En stor del af dette menes at skyldes nedsat produktion af prostaglandiner og TXA2. Aspirins evne til at undertrykke produktionen af prostaglandiner og thromboxaner skyldes dets irreversible inaktivering af enzymet cyclooxygenase (COX). Cyclooxygenase er nødvendig for prostaglandin- og tromboxansyntesen. Aspirin virker som et acetylerende middel, hvor en acetylgruppe er kovalent bundet til en serinrest i COX-enzymets aktive sted. Dette adskiller aspirin fra andre NSAID'er (som f.eks. diclofenac og ibuprofen), som er reversible inhibitorer. Andre virkninger af aspirin, såsom afkobling af oxidativ fosforylering i mitokondrier og modulering af signalering gennem NF-κB, er imidlertid også ved at blive undersøgt. Nogle af aspirins virkninger ligner dem af salicylsyre, som ikke er et acetylerende middel.
Mechanism of action of aspirin
Aspirin causes several different effects in the body, mainly the reduction of inflammation, analgesia (relief of pain), the prevention of clotting, and the reduction of fever. Much of this is believed to be due to decreased production of prostaglandins and TXA2. Aspirin's ability to suppress the production of prostaglandins and thromboxanes is due to its irreversible inactivation of the cyclooxygenase (COX) enzyme. Cyclooxygenase is required for prostaglandin and thromboxane synthesis. Aspirin acts as an acetylating agent where an acetyl group is covalently attached to a serine residue in the active site of the COX enzyme. This makes aspirin different from other NSAIDs (such as diclofenac and ibuprofen), which are reversible inhibitors. However, other effects of aspirin, such as uncoupling oxidative phosphorylation in mitochondria, and the modulation of signaling through NF-κB, are also being investigated. Some of its effects are like those of salicylic acid, which is not an acetylating agent.
Mechanism of action of aspirin