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. 2022 Aug 26;23(1):e22–e33. doi: 10.1016/S1473-3099(22)00433-9

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Prostanoid production and NSAIDs

The 20-carbon fatty acid arachidonic acid is released from membrane phospholipids by phospholipase A₂, which is activated by physical, chemical, and inflammatory stimuli. Arachidonic acid is converted by COX-1 and COX-2 to the unstable intermediate PGH₂. By tissue-specific isomerases, PGH₂ is metabolised to bioactive prostanoids, which include PGE₂, PGD₂, PGF_2α, TxA₂, and PGI₂. After binding to their receptors (EPr_1–4, DPr₁, DPr₂, FP_α, FP_β, TP_α, TP_β, and IP), prostanoids elicit a wide variety of biological effects involved in homoeostatic and normal tissue function but also implicated in pathophysiological processes including infection, thrombosis, and inflammation. The principal therapeutic effect of NSAIDs is related to their capability to inhibit the cyclooxygenase activity of COX-1 and COX-2 enzymes, eventually suppressing the formation of prostanoids. DC=dendritic cell. NSAIDs=non-steroidal anti-inflammatory drugs.