Tanahashi N, Fukuuchi Y, Tomita M, Tomita Y, Inoue K, Satoh H, Abe T
Department of Neurology, School of Medicine, 35 Shinanomachi, Shinjuku-ku, 160-8582, Tokyo, Japan.
Neurosci Lett. 2001 Mar 23;301(1):33-6. doi: 10.1016/s0304-3940(01)01608-1.
Employing video-enhanced contrast (VEC) microscopy, we examined whether TAK-029 (GPIIb/IIIa antagonist) inhibits the adhesion of activated platelets to human brain microvascular endothelial cells (HBEC) in vitro. HBECs were cultured on a coverglass and put in the observation chamber of VEC microscopy. Then, activated platelets by adenosine diphosphate (ADP) (2 microM) were perfused over HBEC at a low shear rate of 10 s(-1) for 30 min and washed out. Platelets adhered directly to HBEC. However, platelet adhesion to HBEC was suppressed when platelet rich plasma with ADP (2 microM) plus TAK-029 (GPIIb/IIIa antagonist; 1 microM) was perfused over HBEC for 30 min and washed out. Anti-GPIbalpha antibody (GUR20-5) did not inhibit adhesion of ADP-activated platelets to HBEC. The above results showed adhesion of ADP-activated platelets to HBEC under flow in vitro is mediated via GPIIb/IIIa
采用视频增强对比度（VEC）显微镜，我们研究了TAK - 029（糖蛋白IIb/IIIa拮抗剂）在体外是否抑制活化血小板与人脑微血管内皮细胞（HBEC）的黏附。将HBEC培养在盖玻片上，并置于VEC显微镜的观察室中。然后，以10 s(-1)的低剪切速率将由二磷酸腺苷（ADP）（2微摩尔）活化的血小板灌注到HBEC上30分钟，然后冲洗掉。血小板直接黏附于HBEC。然而，当含有ADP（2微摩尔）加TAK - 029（糖蛋白IIb/IIIa拮抗剂；1微摩尔）的富血小板血浆灌注到HBEC上30分钟然后冲洗掉时，血小板与HBEC的黏附受到抑制。抗糖蛋白Ibalpha抗体（GUR20 - 5）不抑制ADP活化血小板与HBEC的黏附。上述结果表明，体外流动状态下ADP活化血小板与HBEC的黏附是通过糖蛋白IIb/IIIa介导的
