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Daflon plays a crucial role in the prevention of perivascular edema formation and treatment of venous stasis. This activity can be explained by its antagonist activity against prostaglandin E2 (PgE2) and thromboxane (TxA2) biosynthesis leading to inhibition of inflammatory process. Moreover, it also has a contraction activity on the lymphatic ...
Thromboxane synthase inhibitors inhibit the final enzyme (thromboxane synthase) in the synthesis of thromboxane. Ifetroban is a potent and selective thromboxane receptor antagonist. [10] Dipyridamole antagonizes this receptor too, but has various other mechanisms of antiplatelet activity as well.
Thromboxane A 2 (TXA 2) is generated from prostaglandin H 2 by thromboxane-A synthase in a metabolic reaction which generates approximately equal amounts of 12-hydroxyheptadecatrienoic acid (12-HHT). Aspirin irreversibly inhibits platelet cyclooxygenase 1 preventing the formation of prostaglandin H 2, and therefore TXA 2.
A non-physical standard state is one whose properties are obtained by extrapolation from a physical state (for example, a solid superheated above the normal melting point, or an ideal gas at a condition where the real gas is non-ideal). Metastable liquids and solids are important because some substances can persist and be used in that state ...
U46619 is a stable synthetic analog of the endoperoxide prostaglandin PGH 2 first prepared in 1975, [1] and acts as a thromboxane A 2 (TP) receptor agonist. It potently stimulates TP receptor-mediated, but not other prostaglandin receptor-mediated responses in various in vitro preparations and exhibits many properties similar to thromboxane A 2, including shape change and aggregation of ...
11-Dehydrothromboxane B2 (or 11-dehydro-TXB2) is produced from the breakdown of thromboxane A2.It is released by activated platelets and urine levels of 11-dehydro-TXB2 can be used to monitor the response to aspirin therapy when used to prevent heart disease [1] and in diseases where platelet activation is prominent.
A heme group coordinated to a cysteine residue from the enzyme, thromboxane synthase, is involved in the mechanism. Thromboxane A (TXA) is derived from the prostaglandin H2 (PGH2) molecule. PGH2 contains a relatively weak epidioxy bond, and a possible mechanism is known to involve homolytic cleavage of the epidioxide and a rearrangement to TXA ...
Thromboxane A2 synthesis is the target of the drug aspirin, which inhibits the COX-1 enzyme (the source of thromboxane A2 in platelets). [1] 2-(3,4-Di-hydroxyphenyl)-ethanol (DHPE) is a phenolic component of extra-virgin olive oil. An olive oil fraction containing DHPE can inhibit platelet aggregation and thromboxane B2 formation in vitro. [2]