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Prostaglandin G/H synthase 1 Prostaglandin G/H synthase 1 Prostaglandin G/H synthase 2 Arachidonate 5-lipoxygenase Solute carrier organic anion transporter family member 1B1 Solute carrier organic anion transporter family member 1B3 Solute carrier organic anion transporter family member 2B1 Prostaglandin E synthase Prostacyclin synthase Thromboxane-A synthase Cytosolic phospholipase A2 NADPH azoreductase Mesalazine Mesalazine Balsalazide Balsalazide Prostaglandin H2 Prostaglandin E2 Prostaglandin I2 Thromboxane A2 Arachidonic acid O2 Prostaglandin G2 H2O Mesalazine Leukotriene A4 Heme Heme Fe3+ Calcium Glutathione Heme NADPH Phospholipids Acceptor Reduced acceptor Prostaglandin G/H synthase 2 Heme Heme Heme Calcium Endoplasmic Reticulum Cytosol Extracellular space Mesalazine 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. Epithelial cell Intestine Bacteria of the large intestine The inhibition of arachidonate 5-lipoxygenase decreases the level of leukotriene in the cell. This decreases the inflammation because leukotrienes are potent mediators of inflammation.
Endoplasmic Reticulum PTGS1 PTGS1 PTGS2 ALOX5 SLCO1B1 SLCO1B3 SLCO2B1 PTGES PTGIS TBXAS1 PLA2G4A azr Mesalazine Mesalazine Balsalazide Balsalazide Prostaglandin H2 Prostaglandin E2 Prostaglandin I2 Thromboxane A2 Arachidonic acid Oxygen Prostaglandin G2 Water Mesalazine Leukotriene A4 Phospholipids Acceptor Reduced acceptor PTGS2
PTGS1 PTGS1 PTGS2 ALOX5 SLCO1B1 SLCO1B3 SLCO2B1 PTGES PTGIS TBXAS1 PLA2G4A azr 5-Asa 5-Asa Balsala Balsala PGH2 PGE2 PrstgI2 ThrmbA2 20:4 O2 PGG2 H2O 5-Asa LTA4 Heme Heme Fe3+ Ca2+ GSH Heme NADPH Phosp Accepto RA PTGS2 Heme Heme Heme Ca2+ Endoplasmic Reticulum Cytosol Extracellular space Mesalazine 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. Epithelial cell Intestine Bacteria of the large intestine The inhibition of arachidonate 5-lipoxygenase decreases the level of leukotriene in the cell. This decreases the inflammation because leukotrienes are potent mediators of inflammation.
Endoplasmic Reticulum PTGS1 PTGS1 PTGS2 ALOX5 SLCO1B1 SLCO1B3 SLCO2B1 PTGES PTGIS TBXAS1 PLA2G4A azr 5-Asa 5-Asa Balsala Balsala PGH2 PGE2 PrstgI2 ThrmbA2 20:4 O2 PGG2 H2O 5-Asa LTA4 Phosp Accepto RA PTGS2