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How does the drug Aspirin exert its anti-inflammatory effect at a molecular level?

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Aspirin, also known as acetylsalicylic acid, is a nonsteroidal anti-inflammatory drug  NSAID  that exerts its anti-inflammatory, analgesic, and antipyretic effects primarily through the inhibition of cyclooxygenase  COX  enzymes. There are two main isoforms of COX enzymes: COX-1 and COX-2. These enzymes play a crucial role in the synthesis of prostaglandins, which are lipid mediators involved in various physiological processes, including inflammation, pain, and fever.At the molecular level, aspirin exerts its anti-inflammatory effect by irreversibly acetylating a serine residue  Ser-530  in the active site of the COX enzymes. This acetylation blocks the access of arachidonic acid, a substrate for prostaglandin synthesis, to the active site of the enzyme. As a result, the conversion of arachidonic acid to prostaglandin H2  PGH2  is inhibited. PGH2 is a precursor for the synthesis of other prostaglandins  e.g., PGE2, PGD2, PGF2  and thromboxanes  e.g., TXA2 , which are responsible for promoting inflammation, pain, and fever.By inhibiting the COX enzymes and subsequently reducing the production of prostaglandins and thromboxanes, aspirin effectively reduces inflammation, pain, and fever. It is important to note that aspirin has a greater inhibitory effect on COX-1 than COX-2, which is why it is also known to have antiplatelet effects, as COX-1 is involved in platelet aggregation.
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