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The cyclooxygenase pathway in colonic epithelial cells involves two key enzymes—cyclooxygenase 1 (COX‑1) and cyclooxygenase 2 (COX‑2)—that catalyze the conversion of arachidonic acid into prostaglandins. These lipid mediators play essential roles in regulating inflammation, maintaining mucosal integrity, and modulating immune responses. While COX‑1 is constitutively expressed at stable levels throughout normal colon epithelium, COX‑2 expression is typically absent under normal conditions but becomes highly induced during inflammatory states such as inflammatory bowel disease. The upregulation of COX‑2 has been implicated both in chronic inflammation and tumorigenesis within the colon. Both isoforms are clinically relevant drug targets for anti-inflammatory therapies; however, their inhibition carries distinct safety profiles related to gastrointestinal protection and cardiovascular health[1].
Inhibition of prostaglandin synthesis by blocking enzymatic activity of COX‑1/COX‑2 Reduction of inflammation and pain via decreased prostaglandin production
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