Lipopolysaccharide priming potentiates calcium ionophore stimulated human placental prostaglandin E2 release in vitro.

Eicosanoids Pub Date : 1992-01-01
W Gu, G E Rice, M Michael, S P Brennecke
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Abstract

In this study, the effect of bacterial endotoxin (lipopolysaccharide; LPS) and of LPS priming on the in vitro release of PGE2 from human placental explants was investigated. Both LPS and the calcium ionophore A23187 significantly stimulated PGE2 release (P less than 0.05). Simultaneous exposure of placental explants to both LPS and A23187 revealed no additive or synergistic stimulation of PGE2 release. LPS priming of placental tissue significantly increased A23187-stimulated PGE2 release when compared to non-LPS-primed tissues. The addition of exogenous arachidonic acid (the substrate for PGE2 synthesis) also significantly (P less than 0.05) stimulated PGE2 release. There was, however, no significant further stimulation of PGE2 release following LPS priming in arachidonic acid treated explants. These data suggest that LPS not only increases basal PGE2 release in human placentae, but also potentiates agonist-stimulated PGE2 release, possibly by increasing tissue capacity for endogenous arachidonic acid liberation.

脂多糖引发增强钙离子载体刺激人胎盘前列腺素E2的体外释放。
在本研究中,细菌内毒素(脂多糖;研究了LPS对人胎盘外植体PGE2体外释放的影响。LPS和钙离子载体A23187均能显著促进PGE2的释放(P < 0.05)。胎盘外植体同时暴露于LPS和A23187中,没有发现PGE2释放的附加或协同刺激。与非LPS启动组织相比,LPS启动胎盘组织显著增加a23187刺激的PGE2释放。外源花生四烯酸(合成PGE2的底物)的添加也显著(P < 0.05)刺激了PGE2的释放。然而,在花生四烯酸处理的外植体中,LPS启动后,PGE2的释放没有显著的进一步刺激。这些数据表明,LPS不仅增加了人胎盘中PGE2的基础释放,而且还增强了激动剂刺激的PGE2释放,可能是通过增加组织内源性花生四烯酸释放能力来实现的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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