Abstract：
UNASSIGNED: To explore the role of coagulation and fibrinolytic factors, and the potential mechanism of platelet aggregation in the pathogenesis of retinal vein occlusion.
UNASSIGNED: Coagulation and fibrinolytic parameters in patients with retinal vein occlusion were determined using hemagglutinin and HISCL-5000. Relationships between these elevated parameters and factors representing typical clinical manifestations of retinal vein occlusion were examined, and these parameters were analyzed using a STRING database to indicate the potential role of platelet aggregation. Platelet glycoprotein IIb/IIIa (GPIIb/IIIa) levels were evaluated by flow cytometry after antiplatelet treatment in patients and mouse models. Furthermore, the GPIIb/IIIa ligand fibrinogen in peripheral blood and retina of mouse models was assessed by the turbidimetric method and real-time PCR, respectively.
UNASSIGNED: In patients, significant increases in peripheral blood fibrinogen and GPIIb/IIIa levels were observed (p = 0.0040, p < 0.0001, respectively). A positive correlation was observed between macular thickness (MT) and both fibrinogen and GPIIb/IIIa (r = 0.4528, p = 0.0063; r = 0.3789, p = 0.0427, respectively). After intravitreal injections of anti-vascular endothelial growth factor drugs, a significant reduction in fibrinogen levels was observed (p = 0.0072). In addition, the use of antiplatelet drugs resulted in a significant decrease in GPIIb/IIIa (p < 0.0001). In a mouse model, antiplatelet therapy significantly reduced both peripheral blood and retina fibrinogen levels and the overall rate of vein occlusion 3 days after occlusion (p < 0.0005). In addition, the reduction in GPIIb/IIIa levels after antiplatelet therapy was remarkable.
UNASSIGNED: Fibrinogen and GPIIb/IIIa may be involved in retinal vein occlusion and blocking platelet aggregation may be a new therapeutic approach for retinal vein occlusion.
UNASSIGNED: Coagulation and fibrinolytic parameters in patients with retinal vein occlusion were determined using hemagglutinin and HISCL-5000. Relationships between these elevated parameters and factors representing typical clinical manifestations of retinal vein occlusion were examined, and these parameters were analyzed using a STRING database to indicate the potential role of platelet aggregation. Platelet glycoprotein IIb/IIIa (GPIIb/IIIa) levels were evaluated by flow cytometry after antiplatelet treatment in patients and mouse models. Furthermore, the GPIIb/IIIa ligand fibrinogen in peripheral blood and retina of mouse models was assessed by the turbidimetric method and real-time PCR, respectively.
UNASSIGNED: In patients, significant increases in peripheral blood fibrinogen and GPIIb/IIIa levels were observed (p = 0.0040, p < 0.0001, respectively). A positive correlation was observed between macular thickness (MT) and both fibrinogen and GPIIb/IIIa (r = 0.4528, p = 0.0063; r = 0.3789, p = 0.0427, respectively). After intravitreal injections of anti-vascular endothelial growth factor drugs, a significant reduction in fibrinogen levels was observed (p = 0.0072). In addition, the use of antiplatelet drugs resulted in a significant decrease in GPIIb/IIIa (p < 0.0001). In a mouse model, antiplatelet therapy significantly reduced both peripheral blood and retina fibrinogen levels and the overall rate of vein occlusion 3 days after occlusion (p < 0.0005). In addition, the reduction in GPIIb/IIIa levels after antiplatelet therapy was remarkable.
UNASSIGNED: Fibrinogen and GPIIb/IIIa may be involved in retinal vein occlusion and blocking platelet aggregation may be a new therapeutic approach for retinal vein occlusion.
摘要：
■探讨凝血和纤溶因子的作用，以及血小板聚集在视网膜静脉阻塞发病机制中的潜在机制。
■使用血凝素和HISCL-5000测定视网膜静脉阻塞患者的凝血和纤溶参数。检查了这些升高的参数与代表视网膜静脉阻塞典型临床表现的因素之间的关系，使用STRING数据库分析这些参数,以表明血小板聚集的潜在作用.在患者和小鼠模型中抗血小板治疗后，通过流式细胞术评估血小板糖蛋白IIb/IIIa（GPIIb/IIIa）水平。此外，通过比浊法和实时PCR评估小鼠模型外周血和视网膜中的GPIIb/IIIa配体纤维蛋白原，分别。
■在患者中，观察到外周血纤维蛋白原和GPIIb/IIIa水平显着增加（分别为p=0.0040，p<0.0001）。黄斑厚度（MT）与纤维蛋白原和GPIIb/IIIa之间呈正相关（分别为r=0.4528，p=0.0063；r=0.3789，p=0.0427）。玻璃体内注射抗血管内皮生长因子药物后，观察到纤维蛋白原水平显著降低(p=0.0072).此外,抗血小板药物的使用导致GPIIb/IIIa显著降低(p<0.0001).在老鼠模型中，抗血小板治疗显著降低了闭塞后3天外周血和视网膜纤维蛋白原水平以及静脉闭塞的总发生率(p<0.0005).此外,抗血小板治疗后GPIIb/IIIa水平显著下降.
■纤维蛋白原和GPIIb/IIIa可能参与视网膜静脉阻塞，阻断血小板聚集可能是治疗视网膜静脉阻塞的新方法。
■使用血凝素和HISCL-5000测定视网膜静脉阻塞患者的凝血和纤溶参数。检查了这些升高的参数与代表视网膜静脉阻塞典型临床表现的因素之间的关系，使用STRING数据库分析这些参数,以表明血小板聚集的潜在作用.在患者和小鼠模型中抗血小板治疗后，通过流式细胞术评估血小板糖蛋白IIb/IIIa（GPIIb/IIIa）水平。此外，通过比浊法和实时PCR评估小鼠模型外周血和视网膜中的GPIIb/IIIa配体纤维蛋白原，分别。
■在患者中，观察到外周血纤维蛋白原和GPIIb/IIIa水平显着增加（分别为p=0.0040，p<0.0001）。黄斑厚度（MT）与纤维蛋白原和GPIIb/IIIa之间呈正相关（分别为r=0.4528，p=0.0063；r=0.3789，p=0.0427）。玻璃体内注射抗血管内皮生长因子药物后，观察到纤维蛋白原水平显著降低(p=0.0072).此外,抗血小板药物的使用导致GPIIb/IIIa显著降低(p<0.0001).在老鼠模型中，抗血小板治疗显著降低了闭塞后3天外周血和视网膜纤维蛋白原水平以及静脉闭塞的总发生率(p<0.0005).此外,抗血小板治疗后GPIIb/IIIa水平显著下降.
■纤维蛋白原和GPIIb/IIIa可能参与视网膜静脉阻塞，阻断血小板聚集可能是治疗视网膜静脉阻塞的新方法。
