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[脂多糖毒素增强人血小板对凝血酶刺激的功能反应的能力]

[Ability of a lipopolysaccharide toxin to intensify the functional response of human thrombocytes to thrombin stimulation].

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 Feb;105(2):158-60.

PMID:2832013
Abstract

The preincubation of isolated washed human platelets with lipopolysaccharide toxin (LPS) from Salmonella typhimurium (10 min, 37 degrees) speeds up the thrombin-induced aggregation. Besides, LPS-pretreatment was shown to alter the turnover of polyphosphoinositides stimulated by thrombin and significantly elevated concentrations of diacylglycerol and thromboxane B2 in comparison with control platelets. However, LPS does not influence on the lipid fluidizing effect of thrombin action as testifies by ESR spectroscopy with doxyl-stearic acids as spin-probes. An LPS pretreatment of platelets that induces no aggregation by itself is proposed might transform cells into a state of hidden activation" associated with the accumulation of such products as diacylglycerol and precursors of thromboxane B2. Addition of thrombin to such "preactivated" platelets could cause a more effective aggregation.

摘要

将分离并洗涤过的人血小板与鼠伤寒沙门氏菌的脂多糖毒素(LPS)进行预孵育(10分钟,37摄氏度)可加速凝血酶诱导的聚集。此外,与对照血小板相比,LPS预处理显示可改变凝血酶刺激的多磷酸肌醇的周转,并显著提高二酰基甘油和血栓素B2的浓度。然而,如以多羟基硬脂酸作为自旋探针的电子顺磁共振光谱所证明的,LPS并不影响凝血酶作用的脂质流化效应。有人提出,对血小板进行LPS预处理本身虽不诱导聚集,但可能会使细胞转变为“隐藏激活”状态,这与二酰基甘油和血栓素B2前体等产物的积累有关。向这种“预激活”的血小板中添加凝血酶可能会导致更有效的聚集。

相似文献

1
[Ability of a lipopolysaccharide toxin to intensify the functional response of human thrombocytes to thrombin stimulation].[脂多糖毒素增强人血小板对凝血酶刺激的功能反应的能力]
Biull Eksp Biol Med. 1988 Feb;105(2):158-60.
2
[Phosphoinositide breakdown and diacyl glycerin formation in human thrombocytes as affected by a lipopolysaccharide toxin].[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]
Biull Eksp Biol Med. 1988 Mar;105(3):291-4.
3
Effects of tetanus toxin, Salmonella typhimurium porin, and bacterial lipopolysaccharide on platelet aggregation.破伤风毒素、鼠伤寒沙门氏菌孔蛋白和细菌脂多糖对血小板聚集的影响。
J Med. 1992;23(5):327-38.
4
[The capacity of Yersinia pestis toxin to decrease the functional response of human thrombocytes to stimulation by hormones].
Biull Eksp Biol Med. 1993 Nov;116(11):529-32.
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[Lipopolysaccharide-induced hydrolysis of plasmalogenic phosphatidylethanolamine in human platelets].
Biokhimiia. 1988 May;53(5):842-7.
6
Metabolic properties of human platelet membranes. II. Thrombin-induced phosphorylation of membrane lipids and demonstration of phosphorylating enzymes in the platelet membrane.人血小板膜的代谢特性。II. 凝血酶诱导的膜脂磷酸化及血小板膜中磷酸化酶的证实。
Thromb Haemost. 1976 Apr 30;35(2):364-76.
7
U73122 affects the equilibria between the phosphoinositides as well as phospholipase C activity in unstimulated and thrombin-stimulated human and rabbit platelets.U73122影响未受刺激和凝血酶刺激的人及兔血小板中磷酸肌醇之间的平衡以及磷脂酶C的活性。
J Pharmacol Exp Ther. 1993 Sep;266(3):1156-63.
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Pathways responsible for platelet hypersensitivity in rats with diabetes. I. Streptozocin-induced diabetes.糖尿病大鼠血小板超敏反应的相关通路。I. 链脲佐菌素诱导的糖尿病。
J Lab Clin Med. 1986 Feb;107(2):148-53.
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Functional involvement of thrombospondin in platelet aggregation induced by low versus high concentrations of thrombin.血小板反应蛋白在低浓度与高浓度凝血酶诱导的血小板聚集中的功能参与。
Thromb Haemost. 1986 Feb 28;55(1):136-42.
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[Chemiluminescence of thrombocytes in thrombin-induced aggregation].[凝血酶诱导聚集过程中血小板的化学发光]
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