去纤维钠（去纤苷）是什么药物？

(Defibrotide) 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. It 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, the drug 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.

A foreign study cultured vascular endothelial cells in a matrix containing plasma from patients after autologous HSCT. The results showed that defibrinated sodium 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. DF can significantly inhibit these reactions related to endothelial cell activation and injury, thereby reducing inflammation and inhibiting thrombosis.

Other studies have found that defibrinated sodium can bind to plasmin, increase plasmin activity and promote fibrinolysis, but it cannot activate plasminogen to plasmin. Another study found that bacterial lipopolysaccharide (LPS) can induce the expression of TF in vascular endothelial cells, increase the level of plasminogen activation inhibitor-1 (PAI-1) and reduce the level of tissue plasminogen activator (t-PA), while DF can inhibit these effects of LPS, thereby promoting fibrinolysis. It can also increase the expression of t-PA in resting endothelial cells, enhance fibrinolysis, and avoid fibrin deposition and vascular occlusion.

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