Yamazaki H, Tai H H
Division of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, University of Kentucky, Lexington 40536-0082.
Prostaglandins Leukot Essent Fatty Acids. 1990 May;40(1):51-5. doi: 10.1016/0952-3278(90)90116-3.
PMA is known to enhance calcium ionophore A-23187 induced arachidonate release in human neutrophils. Mechanism of enhancement by PMA is not clear. We have found that neutrophils pretreated with PMA showed significant reduction in labeled arachidonate uptake. Decrease in arachidonate uptake following PMA treatment was attributed, at least in part, to inactivation of arachidonoyl CoA synthase and arachidonoyl CoA lysophosphatide acyltransferase, two key enzymes involved in arachidonate incorporation into phospholipids. These results suggest that PMA may induce protein kinase C activation which in turn may cause inactivation of the two enzymes involved in incorporation of arachidonate resulting in greater availability of arachidonate which is liberated by A-23187 for oxygenation and release into extracellular space.
PMA, 4 beta-phorbol 12-myristate 13-acetate; PDD, 4 alpha-phorbol 12,13-didecanoate; TXB2, thromboxane B2; LTB4, leukotriene B4; PC, phosphatidylcholine; LPC, lysophosphatidylcholine; DMSO, dimethylsulfoxide.
已知佛波酯（PMA）可增强钙离子载体A - 23187诱导的人中性粒细胞花生四烯酸释放。PMA增强作用的机制尚不清楚。我们发现，用PMA预处理的中性粒细胞显示标记的花生四烯酸摄取显著减少。PMA处理后花生四烯酸摄取的减少至少部分归因于花生四烯酰辅酶A合成酶和花生四烯酰辅酶A溶血磷脂酰转移酶的失活，这两种关键酶参与花生四烯酸掺入磷脂。这些结果表明，PMA可能诱导蛋白激酶C活化，进而可能导致参与花生四烯酸掺入的两种酶失活，从而使花生四烯酸有更多可利用性，该花生四烯酸由A - 23187释放用于氧化并释放到细胞外空间。
PMA，4β - 佛波醇12 - 肉豆蔻酸酯13 - 乙酸酯；PDD，4α - 佛波醇12,13 - 十二烷酸酯；TXB2，血栓素B2；LTB4，白三烯B4；PC，磷脂酰胆碱；LPC，溶血磷脂酰胆碱；DMSO，二甲基亚砜。
