去纤维钠（去纤苷）作用功效

(Defitelio) is a mixture of single-stranded oligonucleotides decomposed from genomic DNA from calf lungs or pig intestinal mucosa. The oligonucleotide chain lengths of this drug vary, and the relative molecular mass ranges from 15×10³ to 30×10³. Its purine to pyrimidine ratio is greater than 0.85.

The mechanism of action of defibrotide sodium (defibrinoside) is complex and is not yet fully understood. Preclinical studies have confirmed that defibrinated sodium has anti-thrombotic, fibrinolytic, anti-ischemic and anti-infective effects in vivo and in vitro. Defibrotide sodium is an adenosine receptor agonist with multiple effects. The adenosine A1/A2 receptors of endothelial cells are involved in the regulation of endothelial cells and the response of endothelial cells to injury. Defibrotide sodium can act on these receptors to produce a variety of downstream effects. Defibrinated sodium can also reduce the expression of cell adhesion molecules on the surface of endothelial cells, thereby reducing the adhesion of leukocytes to vascular endothelial cells and reducing the inflammatory damage of endothelial cells. In addition, defibrinated sodium can also promote the release of prostaglandin 12 (PGl2) and prostaglandin E2 (PGE2), thereby causing vasodilation, inhibiting platelet aggregation, and reducing ischemic damage.

Studies have shown that defibrinated sodium can significantly increase the expression of thrombin regulatory protein (TM) and tissue factor pathway inhibitor (TFPI), thereby producing anticoagulant effects. In some inflammatory and ischemic diseases, the imbalance between cathepsin G and its physiological inhibitors can lead to tissue cell destruction and platelet aggregation. Defibrotide sodium can bind to cathepsin G and inhibit its function.

Foreign researchers cultured vascular endothelial cells in a matrix containing plasma from patients after autologous HSCT (HSCT). The results showed that it can increase the expression of intercellular adhesion molecule-1 (ICAM-1) on the surface of vascular endothelial cells, increase the content of tissue factor (TF) and von Willebrand factor in the extracellular matrix, and cause the upregulation of P38MAPK and AKT signaling pathways, thereby reducing inflammation and inhibiting thrombosis.

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