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How does aspirin reduce inflammation by affecting prostaglandin production?

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Pathways of complement activation — inflammation The main function of complement proteins is to aid in the destruction of pathogens by piercing their outer membranes (cell lysis) or by making them more attractive to phagocytic cells such as macrophages (a process known as opsonization). Some complement components also promote inflammation by stimulating cells to release histamine and by attracting phagocytic cells to the site of infection.

Aspirin reduces inflammation by inhibiting the synthesis of prostaglandins, which are potent chemical messengers that mediate inflammatory and immune responses.12

In the body, prostaglandins are synthesized from arachidonic acid through the action of the enzyme cyclooxygenase (COX). During tissue injury or inflammation, this process is activated, leading to the production of prostaglandins that cause local blood vessels to dilate and become more permeable, resulting in the characteristic redness, heat, swelling, and pain associated with inflammation.12

Aspirin acts as a COX inhibitor, effectively blocking the enzyme responsible for converting arachidonic acid into the precursors of prostaglandins. By preventing the production and release of these inflammatory mediators, aspirin suppresses the physiological responses that lead to pain and swelling in local tissues. While this mechanism is highly effective for managing inflammatory conditions, it is also responsible for certain side effects, such as gastric irritation, because prostaglandins also serve protective roles in the gastrointestinal tract.1234