Aspirin inhibits the synthesis of which chemicals that cause inflammation and pain?

Aspirin is commonly known for its role as a non-steroidal anti-inflammatory drug (NSAID), and its primary mechanism of action involves the inhibition of enzymes involved in the synthesis of prostaglandins. Prostaglandins are lipid compounds that have several functions in the body, particularly in response to injury or illness; they are crucial mediators in the inflammatory process, leading to symptoms such as pain, swelling, and fever.

When tissues are damaged or inflamed, prostaglandins are produced and contribute to the sensation of pain by sensitizing nerve endings. They also play a role in the regulation of inflammation and the immune response. By inhibiting the cyclooxygenase (COX) enzymes that facilitate the conversion of arachidonic acid to prostaglandins, aspirin effectively reduces the levels of these inflammatory mediators, thereby alleviating pain and inflammation.

This mechanism highlights why aspirin is used effectively in treating conditions such as arthritis, muscle pain, and other inflammatory disorders. The other options, while involved in various physiological processes related to inflammation and pain, are not directly inhibited by aspirin in the same way as prostaglandins are.