Khan A A, Imai A, Tamaya T
Department of Obstetrics and Gynecology, Gifu University School of Medicine, Japan.
Res Commun Chem Pathol Pharmacol. 1990 Jul;69(1):119-22.
Growing evidence suggests an association between intra-amniotic infection and premature initiation of parturition. We recently demonstrated that some factor(s) including endotoxin produced by the organism stimulates endogenous phospholipase A2 resulting in liberation of arachidonic acid and prostaglandin formation (Arch. Gynecol. Obstet. 244: 1-6 (1988). The studies presented in this report were designated to evaluate the mechanism for endotoxin to stimulate phospholipase A2 using human endometrial fibroblasts. Exposure of the fibroblasts to endotoxin from Escherichia coli in the presence of [32P] phosphate increased 32P-labeling of phosphatidic acid (PA) and phosphatidyl-inositol (PI) in a dose-dependent and a time-dependent manners. The PA labeling occurred without a measurable lag time. These findings demonstrate that the endotoxin stimulates phosphoinositide metabolism in human endometrial fibroblasts by a receptor-mediated mechanism. Membrane phosphoinositide turnover stimulated by endotoxin results in cytosolic Ca2+ increment, liberation of arachidonic acid, which may be involved in the initiation of parturition.
越来越多的证据表明羊膜腔内感染与分娩过早发动之间存在关联。我们最近证明，包括该生物体产生的内毒素在内的某些因素会刺激内源性磷脂酶A2，导致花生四烯酸的释放和前列腺素的形成（《妇产科文献》244: 1 - 6 (1988)）。本报告中的研究旨在利用人子宫内膜成纤维细胞评估内毒素刺激磷脂酶A2的机制。在存在[32P]磷酸盐的情况下，将成纤维细胞暴露于大肠杆菌的内毒素中，会以剂量依赖性和时间依赖性方式增加磷脂酸（PA）和磷脂酰肌醇（PI）的32P标记。PA标记没有可测量的延迟时间就发生了。这些发现表明，内毒素通过受体介导的机制刺激人子宫内膜成纤维细胞中的磷酸肌醇代谢。内毒素刺激的膜磷酸肌醇周转导致胞质Ca2+增加、花生四烯酸的释放，这可能与分娩的发动有关。
