Industry Information

Stability of ulinastatin membrane

  (1) stabilize the cell membrane, prevent the release of inflammatory factors, and block the cascade reaction:

  Acute pancreatitis induces overactivation of mononuclear macrophages and neutrophils, and a large influx of calcium ions phosphorylates extracellular regulatory protein kinase (erk1/2), thereby mediating transcriptional activation of NF- and expression of TNF-a/ il-1. Ulinastatin serine 10 is connected to a chondroitin sulfate sugar chain. On the one hand, it forms chelate with calcium ions to inhibit the flow of calcium ions, block signal transduction, and reduce the production of tnf-a/il-1. On the other hand, it binds to tumor necrosis factor-stimulating gene (tsg-6) to stabilize the cell membrane, inhibit the release of tnf-a/il-1, and block the inflammatory cascade.

Stability of ulinastatin membrane

  (2) stabilize lysosomal membrane, inhibit release and reduce cell damage:

  Under the influence of stimulus factors and other factors, lysosomal membrane is broken, and a variety of lysosomal enzymes such as cathepsin and hyaluronidase are released, causing cell autolysis, and a large number of inflammatory mediators and lysosomal enzymes are released, further causing inflammatory cascade reaction and tissue destruction. Ulinastatin binds to the receptor on macrophages, which can stabilize lysosomal membrane, inhibit lysosomal enzyme release, and reduce cell damage. It stabilizes the cell membrane, inhibits the release of tnf-a/il-1b, and blocks the inflammatory cascade.