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[脂多糖毒素对人血小板中磷酸肌醇分解及二酰甘油形成的影响]

[Phosphoinositide breakdown and diacyl glycerin formation in human thrombocytes as affected by a lipopolysaccharide toxin].

作者信息

Viktorov A V, Dank E Kh, Kuznetsov V A, Ter-Simonian V G, Iurkiv V A

出版信息

Biull Eksp Biol Med. 1988 Mar;105(3):291-4.

PMID:2832017
Abstract

The interaction of lipopolysaccharide toxin (LPS) with isolated washed human blood platelets has been studied. LPS was found to induce the rapid (1-2 min) and marked (15-20%) breakdown of mono- and polyphosphoinositides and formation of significant amounts of diacylglycerols (ca. 20%). However TxB2 biosynthesis from endogenous 14C-arachidonic acid was stimulated by LPS incubation only by ca. 20%. Phosphatidylcholine and phosphatidylethanolamine were also hydrolysed by ca. 8 and 12%, respectively, presumably via the activation of endogenous phospholipase A2. Besides, LPS caused the decreasing of the lipid fluidity of a platelet plasma membrane as was shown by ESR spectroscopy using doxylstearic acid probes. All these changes by LPS induce no aggregation of platelets. It is concluded that an enhancement of a phosphoinositide cycle is not a possibly necessary and sufficient condition for a platelet aggregation.

摘要

已对脂多糖毒素(LPS)与分离的洗涤过的人血血小板之间的相互作用进行了研究。发现LPS可诱导单磷酸和多磷酸肌醇迅速(1 - 2分钟)且显著(15 - 20%)分解,并形成大量二酰基甘油(约20%)。然而,LPS孵育仅使内源性14C - 花生四烯酸生成血栓素B2的生物合成增加约20%。磷脂酰胆碱和磷脂酰乙醇胺也分别被水解约8%和12%,推测是通过内源性磷脂酶A2的激活。此外,如使用硬脂酸多昔洛尔探针通过电子自旋共振光谱法所示,LPS导致血小板质膜的脂质流动性降低。LPS引起的所有这些变化均未诱导血小板聚集。得出的结论是,磷酸肌醇循环的增强并非血小板聚集可能的必要和充分条件。

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