ThromboxaneB2 (TXB2) is a compound significantly released from aggregating platelets and undergoes metabolic transformation during circulation into 11-dehydro TXB2 and 2,3-dinor TXB2. The latter, 2,3-dinor TXB2, serves as a prevalent urinary metabolite of TXB2 and acts as an indicator for in vivo TXA2 synthesis. Studies have shown that in healthy male volunteers, the median excretion rate of 2,3-dinor TXB2 is measured at 10.3 ng hour, equivalent to 138 pg mg of creatinine.
11-Dehydro-2,3-dinor ThromboxaneB2 (11-dehydro-2,3-dinor TXB2) is a metabolite derived from the inactive TXA2 metabolite, TXB2. Its formation involves the action of cytosolic aldehyde dehydrogenase (ALDH) and β-oxidation processes. Remarkably, levels of 11-dehydro-2,3-dinor TXB2 have been observed to increase by 5.2-fold in a surgery-induced rat model of tendon overuse, highlighting its potential role in physiological stress responses.
Thromboxane A2, as an unstable intermediate between the prostaglandin endoperoxides and thromboxaneB2, is a potent inducer of platelet aggregation and causes vasoconstriction.
ThromboxaneB2 (TXB2) is released in substantial quantities from aggregating platelets and metabolized during circulation to 11-dehydro TXB2 and 2,3-dinor TXB2. In rats and rabbits, 2,3-dinor TXB1 has been identified as another urinary metabolite of TXB2. However in human urine, only trace amounts of 2,3-dinor TXB1 have been identified. In rats, 2,3-dinor TXB1 is excreted at a much higher rate than 2,3-dinor TXB2 (19.2 ± 4.9 ng/24 hr and 1.6 ± 0.3 ng/24 hr, respectively). Therefore, urinary 2,3-dinor TXB1 is a suitable marker of thromboxane biosynthesis in rats.
1,2,3-Trilinoelaidoyl-rac-glycerol is a triacylglycerol that contains linoelaidic acid at the sn-1, sn-2, and sn-3 positions. Dietary administration of 1,2,3-trilinoelaidoyl-rac-glycerol (0.6-6.3% w/w) lowers serum levels of thromboxaneB2 , prostaglandin F2 (PGF2), and PGE in rats.1 |1. Bruckner, G., Goswami, S., and Kinsella, J.E. Dietary trilinoelaidate: Effects on organ fatty acid composition, prostanoid biosynthesis and platelet function in rats. J. Nutr. 114(1), 58-67 (1984).
Lornoxicam-d4 is intended for use as an internal standard for the quantification of lornoxicam by GC- or LC-MS. Lornoxicam is a COX inhibitor and non-steroidal anti-inflammatory drug (NSAID) with anti-inflammatory and analgesic properties. It inhibits production of thromboxaneB2 from arachidonic acid in HEL human erythroleukemic cells, which endogenously express COX-1, as well as inhibits LPS-induced formation of prostaglandin F1α from arachidonic acid in Mono-Mac-6 cells, which endogenously express COX-2. Lornoxicam reduces LPS-induced production of nitric oxide and IL-6 in cell-based assays with IC50 values of 65 and 54 µM, respectively. It reduces carrageenan-induced paw edema in rats when administered intravenously at doses ranging from 0.1 to 9 mg kg. Formulations containing lornoxicam have been used in the management of postoperative pain.
Mulberrofuran A can inhibit the formations of 12-hydroxy-, 8, 10-heptadecatrienoic acid (HHT) and thromboxaneB2, but it can increase the formation of 12-hydroxy-5, 8, 10, 14-eicosatetraenoic acid (12-HETE).