输血相关急性肺损伤 z-bo 2021-01-07 273

　　Objective To evaluate the mechanism of ceramide in aging platelets on blood transfusion-related acute lung injury.

　　Method Pre-stimulation with lipopolysaccharide, followed by infusion of 10mL/kg of platelets stored for 1~5d, in BALB/c mice to construct a TRALI second-hit model. Intervention of TRAIL model mice with acid sphingomyelinase specific inhibitor ARC39 or infusion of platelets from acid sphingomyelinase-deficient mice, evaluation of sphingomyelin components in mouse platelets at different time points and lungs of TRAIL model mice The accumulation of neutrophils, endothelial barrier function, lung tissue pathological damage.

　　Results The infusion of platelets stored for 1 to 5 days into C57/B6 mice pre-stimulated with lipopolysaccharides (LPS) can cause the characteristic lung tissue damage, and the severity of the damage increases with the increase of platelet storage time. The ceramide in platelets is continuously accumulated and released during storage. Compared with the control group, infusion of platelets pretreated with ARC39 or platelets lacking acid sphingomyelinase can significantly alleviate lung tissue damage.

　　Conclusion Aging platelets can cause TRALI in mice, but this damage can be reversed and treated by acid sphingomyelinase inhibitors or specifically knocking out the acid sphingomyelinase gene. Interventions for sphingolipid formation are expected to increase blood products Effective strategies for storage safety and longevity.