NSAIDs reduce synthesis of which inflammatory mediators by inhibiting COX enzymes?

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Multiple Choice

NSAIDs reduce synthesis of which inflammatory mediators by inhibiting COX enzymes?

NSAIDs work by blocking cyclooxygenase (COX) enzymes, which are the channels that convert arachidonic acid into prostaglandins and thromboxanes. When COX is inhibited, prostaglandin synthesis drops, and with fewer prostaglandins, inflammation, pain, and fever decrease. Leukotrienes come from a different pathway (lipoxygenase), so their production isn’t directly reduced by COX inhibition. Interleukins are cytokines produced by immune cells, and platelet-derived growth factor is a growth factor; neither is produced directly through the COX pathway. So the inflammatory mediator whose synthesis is reduced by COX inhibition is prostaglandins.

NSAIDs work by blocking cyclooxygenase (COX) enzymes, which are the channels that convert arachidonic acid into prostaglandins and thromboxanes. When COX is inhibited, prostaglandin synthesis drops, and with fewer prostaglandins, inflammation, pain, and fever decrease. Leukotrienes come from a different pathway (lipoxygenase), so their production isn’t directly reduced by COX inhibition. Interleukins are cytokines produced by immune cells, and platelet-derived growth factor is a growth factor; neither is produced directly through the COX pathway. So the inflammatory mediator whose synthesis is reduced by COX inhibition is prostaglandins.

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