Hirafuji M, Nave J F
Merrell-Dow Research Institute, Strasbourg Center, France.
Agents Actions. 1987 Oct;22(1-2):159-64. doi: 10.1007/BF01968832.
In rat basophilic leukemia cells (2 H3-RBL) stimulated with the calcium ionophore A23187, a rapid build-up of PAF-acether was observed within 5 minutes. Thereafter, a slow and complete catabolism was observed within the next 55 minutes. Accumulation of PAF-acether required calcium in the medium and was increased in the presence of acetyl-CoA. Phenyl methyl sulfonyl fluoride, a serine hydrolase inhibitor active on 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine acetyl hydrolase also produced an increased accumulation of PAF-acether in ionophore-stimulated cells. Quinacrine, a non specific inhibitor of phospholipase A2 impaired PAF-acether formation in a dose-dependent manner. The time-course of PAF-acether formation was compared with the ionophore-induced release of arachidonic acid from these cells.
在用钙离子载体A23187刺激的大鼠嗜碱性白血病细胞(2H3-RBL)中,在5分钟内观察到血小板活化因子(PAF-乙醚)迅速积累。此后,在接下来的55分钟内观察到缓慢且完全的分解代谢。PAF-乙醚的积累需要培养基中的钙,并且在乙酰辅酶A存在下会增加。苯甲基磺酰氟是一种对1-O-烷基-2-乙酰基-sn-甘油-3-磷酸胆碱乙酰水解酶有活性的丝氨酸水解酶抑制剂,它也会使离子载体刺激的细胞中PAF-乙醚的积累增加。喹吖因是一种磷脂酶A2的非特异性抑制剂,它以剂量依赖的方式损害PAF-乙醚的形成。将PAF-乙醚形成的时间进程与离子载体诱导的这些细胞中花生四烯酸的释放进行了比较。