Mechanism of action of aspirin

Mechanism of Action of Aspirin

Aspirin, also known as acetylsalicylic acid (acetylsalicylic acid), is a widely used medication with a broad range of therapeutic applications. Its primary mechanism of action involves the inhibition of the cyclooxygenase (COX) enzymes (cyclooxygenase), which play a crucial role in the production of prostaglandins and thromboxanes.

Cyclooxygenase Inhibition

Aspirin exerts its effects by irreversibly inhibiting the COX enzymes. There are two main types of COX enzymes: COX-1 and COX-2. COX-1 is responsible for the production of prostaglandins that protect the stomach lining and regulate blood flow in the kidneys, while COX-2 produces prostaglandins that trigger inflammation and pain.

Aspirin acetylates the serine residue in the active site of the COX enzymes, preventing them from converting arachidonic acid (arachidonic acid) into prostaglandin H2 (prostaglandin H2), the precursor of other prostaglandins and thromboxanes. This inhibition is irreversible, meaning the COX enzymes are permanently deactivated and can no longer produce prostaglandins and thromboxanes.

Anti-Inflammatory Effects

The inhibition of COX-2 leads to a decrease in the production of prostaglandins that mediate inflammation, pain, and fever. This is the basis for aspirin's use as an anti-inflammatory and analgesic (analgesic) agent.

Antiplatelet Effects

Aspirin's ability to inhibit the production of thromboxane A2 (thromboxane A2) by platelets plays a key role in its antiplatelet (antiplatelet) effects. Thromboxane A2 is a potent vasoconstrictor and platelet aggregator, and its inhibition by aspirin results in reduced platelet aggregation and clot formation, which is beneficial in preventing heart attacks and strokes.

Side Effects and Risks

While aspirin's COX-inhibiting effects have therapeutic benefits, they can also lead to side effects. The inhibition of COX-1 can disrupt the protective effects of prostaglandins in the stomach and kidneys, potentially leading to gastrointestinal bleeding and kidney damage.

Conclusion

The mechanism of action of aspirin is complex and multifaceted, involving the irreversible inhibition of the COX enzymes and the subsequent reduction in prostaglandin and thromboxane production. This results in its anti-inflammatory, analgesic, and antiplatelet effects, as well as its potential side effects.

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  3D molecular structure of Aspirin
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  COX-2 enzyme inhibited by Aspirin