Rabson A R, Anderson R, Glover A, Lomnitzer R
Br J Exp Pathol. 1978 Jun;59(3):298-304.
Using Boyden chambers, Prostaglandin A1 (PGA1) was shown to inhibit directed movement of polymorphonuclear (PMN) leucocytes to the chemoattractants endotoxin-activated serum and casein, and in random migration systems. Depressed chemotaxis could not be entirely attributed to defective random migration, as the drug was shown to inhibit both chemokinesis (stimulated random migration) and "true chemotaxis". In addition, PGA1 inhibited the movement of neutrophils out of capillary tubes and substantially reduced hexose monophosphate shunt (HMPS) activity. Mice injected with PGA1 demonstrated significantly less PMN movement into trypticase-soy-broth-induced peritoneal exudates, and it is postulated that during inflammatory processes release of PGA1 increases cell accumulation at the site, thereby amplifying the inflammatory response.
使用博伊登小室法发现，前列腺素A1（PGA1）可抑制多形核（PMN）白细胞向趋化因子内毒素激活血清和酪蛋白的定向移动，以及在随机迁移系统中的移动。趋化性降低不能完全归因于随机迁移缺陷，因为该药物显示可抑制趋化运动（刺激的随机迁移）和“真正的趋化性”。此外，PGA1抑制中性粒细胞从毛细管中移出，并显著降低己糖磷酸旁路（HMPS）活性。注射PGA1的小鼠向胰蛋白酶大豆肉汤诱导的腹腔渗出物中迁移的PMN明显减少，据推测，在炎症过程中PGA1的释放增加了细胞在该部位的聚集，从而放大了炎症反应。
