动物造模,输血相关急性肺损伤 z-bio 2021-12-01 485

　　Objective: To investigate the role of ceramide in blood transfusion-related acute lung injury in senescent platelets.

　　Method: The second attack model of TRALI was constructed in BALB/c mice by injecting 10 mL/kg of platelets after pre-stimulation with lipopolysaccharide and storing them for 1-5 days. Neutrophils intervene in TRAIL model mice by injecting platelets from acid sphingomyelinase specific inhibitor ARC39 or acid sphingomyelinase-deficient mice to evaluate mouse platelets in the lungs of TRAIL model mice at different time points. Sphingomyelin composition, degree of accumulation of globules, endothelial barrier function, and histopathological damage to the lung.

　　Results: Injecting platelets stored for 1-5 days into C57/B6 mice pre-stimulated with lipopolysaccharide (LPS) will cause characteristic damage to lung tissue. The severity of damage is platelets, which increases with the increase of storage time. . Ceramide in platelets continues to accumulate and release during storage. Compared with the control group, injection of platelets pretreated with ARC39 or lacking acid sphingomyelinase can significantly reduce lung tissue damage.

　　Conclusion: Platelet senescence can cause TRALI in mice, but this damage can be eliminated by specifically knocking out acid sphingomyelinase inhibitors or acid sphingomyelinase genes. The intervention of sphingolipid formation is expected to be an effective strategy to improve the safety and longevity of blood products.