Galbraith G M
Department of Microbiology and Immunology, Medical University of South Carolina, Charleston 29425.
Immunopharmacology. 1988 Sep-Oct;16(2):63-9. doi: 10.1016/0162-3109(88)90014-8.
Arachidonic acid mobilization in human polymorphonuclear leukocytes stimulated with calcium ionophore A23187 was amplified by synthetic diacylglycerol and, to a much lesser extent, by phorbol ester. The effect was synergistic and dependent upon influx of calcium ions. Thin layer chromatographic analysis of phospholipids of stimulated cells revealed a loss of arachidonic acid associated with phosphatidylinositol and phosphatidylcholine. The synergistic response was unaffected by treatment of cells with two inhibitors of protein kinase C, namely, polymyxin B and 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine. Moreover, both agents consistently augmented the cellular response to A23187 alone. These findings suggest that A23187-induced arachidonic acid mobilization in leukocytes is independent of protein kinase C activity.
钙离子载体A23187刺激的人多形核白细胞中花生四烯酸的动员可被合成二酰基甘油增强,在较小程度上也可被佛波酯增强。这种作用是协同的,且依赖于钙离子的内流。对受刺激细胞的磷脂进行薄层色谱分析显示,与磷脂酰肌醇和磷脂酰胆碱相关的花生四烯酸有所减少。两种蛋白激酶C抑制剂,即多粘菌素B和1-(5-异喹啉磺酰基)-2-甲基哌嗪对细胞的处理,并未影响这种协同反应。此外,这两种药物均持续增强细胞对单独A23187的反应。这些发现表明,白细胞中A23187诱导的花生四烯酸动员与蛋白激酶C活性无关。