2 results about "Activated coagulation factor" patented technology

This invention discloses a gelatin-based hemostatic powder with high osmotic pressure properties and its preparation method. The hemostatic powder is a porous gelatin-based material grafted with high-osmotic-pressure anionic functional groups such as sulfonic acid groups or their derivatives. The sulfonic acid groups or their derivatives endow the hemostatic powder with negative charge and high osmotic pressure properties, thereby achieving a dual hemostatic effect of osmotic pressure-driven blood concentration and negative charge enrichment to activate coagulation factors. The strong dissociation properties of the sulfonic acid groups or their derivatives endow the material with a surface negative potential of -20 to -50 mV and a high osmotic pressure of 0.30 to 0.55 Osmol / kg, achieving a pressure of 40 to 60 g·g. ‑ ¹ water absorption ratio and 0.15–0.20 g·g ‑ ¹·min ‑ ¹ Rapid water absorption. The preparation method of this invention involves activating the carboxyl group of gelatin and grafting a functional monomer containing a primary amino group, followed by purification, freeze-drying, and grinding. This invention achieves dual hemostatic effects of osmotic pressure-driven blood concentration and negatively charged enrichment to activate coagulation factors, making it suitable for wound hemostasis of arterial, venous, and organ bleeding.

This invention discloses the use of substances that interfere with the expression of coagulation factor X (F10) or inhibit the activity of its activated form, activated coagulation factor X (FXa), in the preparation of drugs for the prevention or treatment of abdominal aortic aneurysm (AAA), belonging to the field of biomedicine. This invention is the first to discover that endothelial-derived F10 / FXa is significantly upregulated in the early stages of AAA development. FXa can disrupt the stability of the endothelial tight junction protein ZO-1 through a non-coagulation-dependent pathway, driving vascular barrier dysfunction and AAA progression. In vivo experiments have confirmed that inhibiting F10 expression or FXa activity can significantly reduce the AAA tumorigenesis rate and inhibit aortic dilation, providing a novel target and intervention strategy for the early prevention and drug treatment of AAA.