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Prostaglandin-endoperoxide synthase 1 and 2, commonly known as COX-1 and COX-2, are key enzymes responsible for the conversion of arachidonic acid into prostaglandin H2, the precursor for various prostanoids including prostaglandins, prostacyclins, and thromboxanes [1, 5, 11]. COX-1 is constitutively expressed in most tissues and plays a vital role in maintaining physiological homeostasis, such as protecting the gastric mucosa and regulating platelet aggregation [7, 8, 12]. In contrast, COX-2 is primarily an inducible enzyme that is upregulated during inflammatory responses, mediating pain, fever, and swelling [9, 10, 16]. Ibuprofen is a non-selective, reversible inhibitor of both isoforms, widely utilized for its analgesic, anti-inflammatory, and antipyretic effects [1, 2, 17]. While effective for symptom management, the inhibition of COX-1 is associated with gastrointestinal toxicity, while the disruption of the prostanoid balance can lead to cardiovascular and renal complications [3, 6, 13, 18].
Reversible, non-selective inhibition of COX-1 and COX-2 enzymes, blocking the conversion of arachidonic acid to prostaglandin H2 (PGH2) [1, 4, 13, 17].
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