Proceedings of the International scientific and practical conference ― Cambridge Science and Education Conference‖ (February 23-25, 2026) / Publisher website: www.naukainfo.com. – Cambridge, United Kingdom, 2026. - 289 p.

75 activities). This catalytic domain contains an arginine residue at position 120 (Arg120), which is required for substrate binding and the inhibitory action of NSAIDs (nonsteroidal anti-inflammatory drugs)[7]. Both COX enzymes promote the oxygenation and cyclization of arachidonic acid to form PGG2, which is then rapidly modified by the peroxidase portion of COX to PGH2. PGH2, being very unstable, is rapidly converted to PGs (PGE2, PGF2α, and PGD2), prostacyclin (PGI2), and thromboxane A2. In platelets, this pathway leads to the formation of thromboxane A2 (TXA2), in vascular endothelium to prostacyclin (PGI2), and in mast cells to PGD2, while in blood vessels, the digestive tract, the lungs, and other tissues to PGE2 (PGF is formed primarily in the smooth muscle of the digestive tract, bronchi, uterus, and blood vessels). All prostanoids then undergo rapid oxidative metabolism to their respective inactive metabolites. The half-life of most PGs in the circulation is less than one minute. Based on the five classes of naturally occurring prostanoids (PGD2, PGE2, PGF2α, PGI2, and TXA2), five major classes of prostanoid receptors have been identified, termed DP, EP, FP, IP, and TP receptors, respectively.[30] EP receptors are divided into four subgroups: EP1, EP2, EP3, and EP4.[31] All of these receptors are G protein-coupled receptors that utilize IP3/DAG or cAMP transduction mechanisms [8]. PGI2 effectively inhibits platelet aggregation. PGD2 and PGE2 also have antiplatelet properties, but PGE2 has inconsistent effects. TXA2 is a potent stimulator of platelet aggregation. Working together with PGI2, it maintains the integrity of the vascular endothelium, preventing platelet aggregation and adhesion to arteriolar walls. Because platelets lack nuclei (and therefore DNA), they cannot continuously synthesize COX-1, and therefore limited amounts of COX-1 and TXA2 are only maintained for the life of the platelet (approximately 7 days). This is in contrast to vascular endothelial cells, which have nuclei and can therefore regularly produce new COX-1 (and therefore PGI2) [8]. PGs play a complex and multifaceted role in the pathogenesis of myeloproliferative neoplasms (MPNs), including involvement in the following processes: