Tag: Cox 1

Non-selective Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) represent a class of medication widely used for pain and inflammation, with their efficacy stemming from the inhibition of both COX-1 and COX-2 enzymes. This dual action, however, also underlies the potential for a range of side effects, particularly affecting the gastrointestinal system. Understanding the distinction between COX-1 and COX-2 is crucial for comprehending how these common drugs function in the body.

Over 29 million Americans use NSAIDs daily for pain, fever, and inflammation. A key question in their pharmacology is, do salicylates block COX-1? The answer depends on the specific type of salicylate and the dose administered.

Every day, millions of people worldwide take low-dose aspirin to help prevent heart attacks and strokes. This preventative effect is directly related to **which blood component does aspirin affect**, primarily targeting the blood's tiny clotting cells known as platelets.

In 1971, researchers led by Sir John Vane discovered that aspirin's primary mechanism of action involves inhibiting an enzyme called cyclooxygenase (COX), which is responsible for producing inflammatory mediators. This groundbreaking discovery revealed precisely what enzyme does aspirin affect and fundamentally changed our understanding of how aspirin works to relieve pain, reduce fever, and prevent blood clots.

Aspirin starts its antiplatelet effects within 60 minutes of ingestion, although the duration of its impact lasts much longer due to its irreversible action on platelets. Understanding **how long does it take for aspirin to affect platelets** involves exploring its unique mechanism of action and the biology of these essential blood cells.