The anti-inflammatory effect of aspirin is due to:
- a- An anticoagulant effect
- b- Inhibition of the synthesis of prostaglandins***
- c- An antigen-antibody reaction
- d- All of the above.
The answer is: (b) Inhibition of the synthesis of prostaglandins.
Aspirin is a nonsteroidal anti-inflammatory drug (NSAID) that works by inhibiting the synthesis of prostaglandins. Prostaglandins are chemicals that are involved in inflammation, pain, and fever. By inhibiting the synthesis of prostaglandins, aspirin can reduce inflammation, pain, and fever.
Aspirin also has an anticoagulant effect, but this is not the main reason for its anti-inflammatory effect.
Antigen-antibody reactions are involved in the immune system, but they are not directly involved in the anti-inflammatory effect of aspirin.
Here is a more detailed explanation of how aspirin works to inhibit the synthesis of prostaglandins:
Prostaglandins are produced by the enzyme cyclooxygenase (COX). There are two main isoforms of COX: COX-1 and COX-2. COX-1 is involved in normal physiological functions, such as maintaining the lining of the stomach and regulating blood flow. COX-2 is induced by inflammation and is involved in the production of inflammatory prostaglandins.
Aspirin inhibits both COX-1 and COX-2, but it has a greater affinity for COX-2. This is why aspirin is effective at reducing inflammation.
However, the inhibition of COX-1 by aspirin can also cause side effects, such as stomach upset and bleeding. To reduce the risk of these side effects, it is important to take aspirin with food and to use the lowest effective dose.
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