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Prostaglandin G/H synthase 1 Prostaglandin G/H synthase 1 Prostaglandin G/H synthase 2 Solute carrier family 22 member 6 Prostaglandin E synthase Prostacyclin synthase Thromboxane-A synthase Cytosolic phospholipase A2 UDP- glucuronosyltransferase 2B7 Indomethacin Indomethacin Indomethacin Acemetacin Acemetacin Prostaglandin H2 Prostaglandin E2 Prostaglandin I2 Thromboxane A2 Arachidonic acid O2 Prostaglandin G2 H2O Heme Heme Glutathione Heme Phospholipids Acceptor Reduced acceptor Prostaglandin G/H synthase 2 Heme Heme Heme Calcium Endoplasmic Reticulum Cytosol Indomethacin inhibits COX-1 (prostaglandin G/H synthase 1) and COX-2 (prostaglandin G/H synthase 2) on the endoplasmic reticulum membrane, preventing the conversion of arachidonic acid into PGH2. Prostaglandin H2 synthesis is reduced COX-1 synthesizes prostaglandins necessary for normal gastrointestinal and renal function. COX-2 is responsible for prostaglandin synthesis during tissue injury and inflammation. Inhibition of COX-2 provides anti-inflammatory activity. Prostaglandin E2 is responsible for inflammation and pain by activating immune cells and stimulating pain fibres. Lower concentrations of prostaglandin E2 lowers inflammatory and pain response, hence an analgesic effect is seen. Decreasing PGE2 in the central nervous system also has an antipyretic effect. Blood vessel Liver Hepatocyte Acemetacin is metabolized in the liver by the hepatic first-pass effect resulting in the formation of Indomethacin by esterolytic cleavage. Human Cell
Endoplasmic Reticulum Endoplasmic Reticulum PTGS1 PTGS1 PTGS2 SLC22A6 PTGES PTGIS TBXAS1 PLA2G4A UGT2B7 Indomethacin Indomethacin Indomethacin Acemetacin Acemetacin Prostaglandin H2 Prostaglandin E2 Prostaglandin I2 Thromboxane A2 Arachidonic acid Oxygen Prostaglandin G2 Water Phospholipids Acceptor Reduced acceptor PTGS2
PTGS1 PTGS1 PTGS2 SLC22A6 PTGES PTGIS TBXAS1 PLA2G4A UGT2B7 Indomet Indomet Indomet Aceme Aceme PGH2 PGE2 PrstgI2 ThrmbA2 20:4 O2 PGG2 H2O Heme Heme GSH Heme Phosp Accepto RA PTGS2 Heme Heme Heme Ca2+ Endoplasmic Reticulum Cytosol Indomethacin inhibits COX-1 (prostaglandin G/H synthase 1) and COX-2 (prostaglandin G/H synthase 2) on the endoplasmic reticulum membrane, preventing the conversion of arachidonic acid into PGH2. Prostaglandin H2 synthesis is reduced COX-1 synthesizes prostaglandins necessary for normal gastrointestinal and renal function. COX-2 is responsible for prostaglandin synthesis during tissue injury and inflammation. Inhibition of COX-2 provides anti-inflammatory activity. Prostaglandin E2 is responsible for inflammation and pain by activating immune cells and stimulating pain fibres. Lower concentrations of prostaglandin E2 lowers inflammatory and pain response, hence an analgesic effect is seen. Decreasing PGE2 in the central nervous system also has an antipyretic effect. Blood vessel Liver Hepatocyte Acemetacin is metabolized in the liver by the hepatic first-pass effect resulting in the formation of Indomethacin by esterolytic cleavage. Human Cell
Endoplasmic Reticulum Endoplasmic Reticulum PTGS1 PTGS1 PTGS2 SLC22A6 PTGES PTGIS TBXAS1 PLA2G4A UGT2B7 Indomet Indomet Indomet Aceme Aceme PGH2 PGE2 PrstgI2 ThrmbA2 20:4 O2 PGG2 H2O Phosp Accepto RA PTGS2