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How does the drug aspirin exert its anti-inflammatory effect at the molecular level, and what is the role of the active ingredient in this process?

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Aspirin, also known as acetylsalicylic acid, exerts its anti-inflammatory effect at the molecular level by inhibiting the production of prostaglandins. Prostaglandins are hormone-like substances that play a crucial role in the inflammatory response, causing pain, fever, and swelling.The active ingredient in aspirin, acetylsalicylic acid, is responsible for this anti-inflammatory effect. It works by irreversibly inhibiting the enzyme cyclooxygenase  COX , which is involved in the synthesis of prostaglandins from arachidonic acid. There are two main isoforms of COX: COX-1 and COX-2. COX-1 is constitutively expressed in most tissues and is involved in the production of prostaglandins that regulate physiological functions, such as gastric mucosal protection and platelet aggregation. COX-2 is induced during inflammation and is responsible for the production of prostaglandins that mediate pain, fever, and swelling.Aspirin acetylates a serine residue in the active site of both COX-1 and COX-2, which prevents the access of arachidonic acid to the active site and thus inhibits the production of prostaglandins. This inhibition of prostaglandin synthesis results in the reduction of inflammation, pain, and fever.In summary, aspirin's anti-inflammatory effect at the molecular level is due to the inhibition of prostaglandin synthesis by the active ingredient, acetylsalicylic acid, which blocks the activity of the COX enzymes. This leads to a decrease in the production of inflammatory prostaglandins, ultimately reducing inflammation, pain, and fever.
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