Saito H, Hirai A, Tamura Y, Yoshida S
Prostaglandins Leukot Med. 1985 Jun;18(3):271-86. doi: 10.1016/0262-1746(85)90059-9.
The effect of 5-lipoxygenase products of arachidonic acid on 14-C-alkyl-acetyl-glycero-phosphocholine (14C-alkyl-acetyl GPC) production in rat peritoneal macrophages was investigated, using macrophages prelabeled with N-methyl-14C-alkyl-lyso-glycero-phosphocholine (14C-alkyl-lyso GPC) (prelabeled macrophages). Bromophenacyl bromide (BPB: phospholipase A2 inhibitor), and AA861 (5-lipoxygenase inhibitor) suppressed the production of 14C-alkyl-acetyl GPC in the A23187-stimulated prelabeled macrophages in a dose-dependent manner. A23187-induced hydrolysis of 14C-alkyl-acyl-glycero-phosphocholine (14C-alkyl-acyl GPC) and formation of 14C-alkyl-lyso GPC were also reduced by BPB and AA861. However, indomethacin (IND: cyclo-oxygenase inhibitor) had no significant effect on 14C-alkyl-acetyl GPC production in the A23187-stimulated prelabeled macrophages. Exogenously supplied 5-hydroperoxy-6,8,11,14-eicosatetraenoic acid (5-HPETE) and 5-hydroxy-6,8,11,14-eicosatetraenoic acid (5-HETE) reversed the inhibitory effect of AA861 on 14C-alkyl-acetyl GPC production in A23187-stimulated prelabeled macrophages. Reduced hydrolysis of 14C-alkyl-acyl GPC and formation of 14C-alkyl-lyso GPC in A23187-stimulated prelabeled macrophages, which were pretreated with AA861, were also reversed by the addition of 5-HPETE and 5-HETE. However, LTB4 had no such effects. 5-HPETE and 5-HETE augmented the stimulatory effect of A23187 on 14C-alkyl-acetyl GPC production in prelabeled macrophages, while they could not stimulate alkyl-acetyl GPC production in the absence of A23187. These results suggest that 5-lipoxygenase products, especially 5-HPETE and 5-HETE, may play an important role in alkyl-acetyl GPC production in rat peritoneal macrophages.
研究了花生四烯酸的5-脂氧合酶产物对大鼠腹腔巨噬细胞中14-C-烷基-乙酰甘油磷酸胆碱（14C-烷基-乙酰甘油磷酸胆碱）生成的影响，使用预先用N-甲基-14C-烷基溶血甘油磷酸胆碱（14C-烷基溶血甘油磷酸胆碱）标记的巨噬细胞（预先标记的巨噬细胞）。溴苯甲酰溴（BPB：磷脂酶A2抑制剂）和AA861（5-脂氧合酶抑制剂）以剂量依赖性方式抑制A23187刺激的预先标记的巨噬细胞中14C-烷基-乙酰甘油磷酸胆碱的生成。BPB和AA861也降低了A23187诱导的14C-烷基酰基甘油磷酸胆碱（14C-烷基酰基甘油磷酸胆碱）的水解和14C-烷基溶血甘油磷酸胆碱的形成。然而，吲哚美辛（IND：环氧化酶抑制剂）对A23187刺激的预先标记的巨噬细胞中14C-烷基-乙酰甘油磷酸胆碱的生成没有显著影响。外源性供应的5-氢过氧-6,8,11,14-二十碳四烯酸（5-HPETE）和5-羟基-6,8,11,14-二十碳四烯酸（5-HETE）逆转了AA861对A23187刺激的预先标记的巨噬细胞中14C-烷基-乙酰甘油磷酸胆碱生成的抑制作用。在预先用AA861处理的A23187刺激的预先标记的巨噬细胞中，14C-烷基酰基甘油磷酸胆碱水解的减少和14C-烷基溶血甘油磷酸胆碱的形成也通过添加5-HPETE和5-HETE而逆转。然而，白三烯B4没有这种作用。5-HPETE和5-HETE增强了A23187对预先标记的巨噬细胞中14C-烷基-乙酰甘油磷酸胆碱生成的刺激作用，而在没有A23187的情况下它们不能刺激烷基-乙酰甘油磷酸胆碱的生成。这些结果表明，5-脂氧合酶产物，尤其是5-HPETE和5-HETE，可能在大鼠腹腔巨噬细胞中烷基-乙酰甘油磷酸胆碱的生成中起重要作用。
