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Prostaglandin G/H synthase 1 Prostaglandin G/H synthase 1 Fibrinogen alpha chain Fibrinogen beta chain Fibrinogen gamma chain Integrin alpha-IIb Integrin beta-3 von Willebrand factor Adenosine receptor A2b Adenylate Cyclase cAMP-specific 3',5'-cyclic phosphodiesterase 4D Thromboxane-A synthase Cytosolic phospholipase A2 Prostaglandin G/H synthase 2 Adenosine receptor A2a Triflusal Adenosine Thromboxane A2 Triflusal Triflusal Prostaglandin H2 Arachidonic acid O2 Prostaglandin G2 H2O ATP cAMP AMP Heme Magnesium Heme Phospholipids Acceptor Reduced acceptor Prostaglandin G/H synthase 2 Heme Heme Calcium Mobilization Zinc (II) ion Heme Calcium Dense Tubular System Blood Vessel Triflusal inhibits COX-1 (prostaglandin G/H synthase 1) on the dense tubular system (DTS), 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. Platelet The inhibition of the calcium mobilization results in the IIb/IIIa receptor to not binds fibrinogen and/or vW factor. In conseuqnece, there is no platelet adhesion and aggrefation possible, thus preventing blood clot. The low level of thromboxane A2 causes a decrease in the activity of the adenylate cyclase, thus there is les cAMP in the platelets. This results in the decrease of the calcium mobilization by the protein kinase A (PKA). Triflusal inhibits the cGMP specific 3',5'-cyclic phosphodiesterase. This causes an increase in the concentratiion of cAMP in the platelet cell. High concentrations of cAMP inhibits platelet activation and aggregation. cAMP also inhibits arachidonic acid being released from the membrane phospholipids further preventing blood clot formation.
Melanosome Endoplasmic Reticulum PTGS1 PTGS1 Unknown Unknown FGG ITGA2B Unknown VWF ADORA2B ADCY10 PDE4D TBXAS1 PLA2G4A PTGS2 ADORA2A Triflusal Adenosine Thromboxane A2 Triflusal Triflusal Prostaglandin H2 Arachidonic acid Oxygen Prostaglandin G2 Water Adenosine triphosphate cAMP Adenosine monophosphate Phospholipids Acceptor Reduced acceptor PTGS2 Calcium Mobilization
PTGS1 PTGS1 FGG ITGA2B VWF ADORA2B ADCY10 PDE4D TBXAS1 PLA2G4A PTGS2 ADORA2A Trifl Adenosi ThrmbA2 Trifl Trifl PGH2 20:4 O2 PGG2 H2O ATP cAMP AMP Heme Mg2+ Heme Phosp Accepto RA PTGS2 Heme Heme Cal Mob Zinc Heme Ca2+ Dense Tubular System Blood Vessel Triflusal inhibits COX-1 (prostaglandin G/H synthase 1) on the dense tubular system (DTS), 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. Platelet The inhibition of the calcium mobilization results in the IIb/IIIa receptor to not binds fibrinogen and/or vW factor. In conseuqnece, there is no platelet adhesion and aggrefation possible, thus preventing blood clot. The low level of thromboxane A2 causes a decrease in the activity of the adenylate cyclase, thus there is les cAMP in the platelets. This results in the decrease of the calcium mobilization by the protein kinase A (PKA). Triflusal inhibits the cGMP specific 3',5'-cyclic phosphodiesterase. This causes an increase in the concentratiion of cAMP in the platelet cell. High concentrations of cAMP inhibits platelet activation and aggregation. cAMP also inhibits arachidonic acid being released from the membrane phospholipids further preventing blood clot formation.
Melanosome Endoplasmic Reticulum PTGS1 PTGS1 FGG ITGA2B VWF ADORA2B ADCY10 PDE4D TBXAS1 PLA2G4A PTGS2 ADORA2A Trifl Adenosi ThrmbA2 Trifl Trifl PGH2 20:4 O2 PGG2 H2O ATP cAMP AMP Phosp Accepto RA PTGS2 Cal Mob