What is the mechanism of action of aspirin?

Aspirin primarily acts through the inhibition of cyclooxygenase (COX) enzymes, specifically COX-1 and COX-2. These enzymes are crucial in the biochemical pathway that leads to the production of prostaglandins and thromboxanes, which are mediators involved in inflammation, pain, and fever.

By inhibiting COX enzymes, aspirin effectively reduces the synthesis of these inflammatory mediators. This mechanism helps relieve pain and decrease inflammation, making aspirin a widely used nonsteroidal anti-inflammatory drug (NSAID). Additionally, the inhibition of COX-1 specifically impacts the production of thromboxane A2, a substance that promotes platelet aggregation. This is why aspirin is also used for its antiplatelet effects, which can help reduce the risk of heart attacks and strokes.

While promoting vasodilation and stimulating prostaglandin production are related to other processes in the body, they do not accurately describe aspirin's primary mechanism. Aspirin does not act as a direct vasodilator, nor does it stimulate prostaglandin production; rather, it prevents their formation. Although aspirin has effects on platelet aggregation, its broader mechanism encompassing inflammation and pain relief is due to its action on the COX enzymes.