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Prostaglandin G/H synthase 1 Prostaglandin G/H synthase 2 Prostaglandin G/H synthase 1 Prostacyclin synthase Phenylbutazone Transporter Prostaglandin E synthase Thromboxane-A synthase Cytosolic phospholipase A2 Phenylbutazone Phenylbutazone Phenylbutazone Prostaglandin H2 Prostaglandin E2 Prostaglandin I2 Thromboxane A2 Arachidonic acid O2 Prostaglandin G2 H2O Heme Heme Heme Glutathione Phospholipids Acceptor Reduced acceptor Prostaglandin G/H synthase 2 Heme Heme Heme Calcium Endoplasmic Reticulum Cytosol Blood vessel Phenylbutazone 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. Also, the production of prostaglandin I2 i even more reduced by the direct inhibition of phenylbutazone on the prostacyclin synthase. 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. Inflamed Cell
Endoplasmic Reticulum PTGS1 PTGS2 PTGS1 PTGIS Unknown PTGES TBXAS1 PLA2G4A Phenylbutazone Phenylbutazone Phenylbutazone Prostaglandin H2 Prostaglandin E2 Prostaglandin I2 Thromboxane A2 Arachidonic acid Oxygen Prostaglandin G2 Water Phospholipids Acceptor Reduced acceptor PTGS2
PTGS1 PTGS2 PTGS1 PTGIS PTGES TBXAS1 PLA2G4A Phbut Phbut Phbut PGH2 PGE2 PrstgI2 ThrmbA2 20:4 O2 PGG2 H2O Heme Heme Heme GSH Phosp Accepto RA PTGS2 Heme Heme Heme Ca2+ Endoplasmic Reticulum Cytosol Blood vessel Phenylbutazone 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. Also, the production of prostaglandin I2 i even more reduced by the direct inhibition of phenylbutazone on the prostacyclin synthase. 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. Inflamed Cell
Endoplasmic Reticulum PTGS1 PTGS2 PTGS1 PTGIS PTGES TBXAS1 PLA2G4A Phbut Phbut Phbut PGH2 PGE2 PrstgI2 ThrmbA2 20:4 O2 PGG2 H2O Phosp Accepto RA PTGS2