What is the mechanism of action of non-steroidal anti-inflammatory drugs (NSAIDs)?

Non-steroidal anti-inflammatory drugs (NSAIDs) primarily function by inhibiting the cyclooxygenase (COX) enzymes, which are crucial in the biosynthesis of prostaglandins. Prostaglandins are lipid compounds that play a significant role in inflammation, pain modulation, and fever. By inhibiting the COX enzymes, NSAIDs decrease the formation of these prostaglandins, leading to reduced inflammation, alleviation of pain, and, often, lowered fever.

The COX family consists of two main enzymes: COX-1 and COX-2. COX-1 is involved in the production of prostaglandins that maintain normal physiological functions, such as protecting the gastric mucosa and promoting platelet aggregation. COX-2, on the other hand, is induced during inflammatory processes, leading to increased levels of prostaglandins associated with pain and inflammation. Therefore, NSAIDs exert their therapeutic effects by selectively inhibiting either or both of these COX enzymes, providing symptomatic relief for various inflammatory conditions.

In contrast, the other options do not accurately reflect the mechanism of action of NSAIDs. Enhancing the production of prostaglandins would increase inflammation and pain, contradicting the therapeutic intent of NSA