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首页> 外文期刊>Platelets >Inhibition of glutamate receptors reduces the homocysteine-induced whole blood platelet aggregation but does not affect superoxide anion generation or platelet membrane fluidization
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Inhibition of glutamate receptors reduces the homocysteine-induced whole blood platelet aggregation but does not affect superoxide anion generation or platelet membrane fluidization

机译：抑制谷氨酸受体降低了同型血小板血小板聚集，但不影响超氧化物阴离子产生或血小板膜流化

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摘要

Homocysteine (Hcy) is an excitotoxic amino acid. It is potentially possible to prevent Hcy-induced toxicity, including haemostatic impairments, by antagonizing glutaminergic receptors. Using impedance aggregometry with arachidonate and collagen as platelet agonists, we tested whether the blockade of platelet NMDA (N-methyl-D-aspartate), AMPA (a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) and kainate receptors with their inhibitors: MK-801 (dizocilpine hydrogen maleate, [5R,10514-1-1-5-methyl-10,11-dihydro-5Hdibenzo(a,d]cyclohepten-5,10-imine), CNQX (7-nitro-2,3-dioxo-1,4-dihydroquinoxaline-6carbonitrile) and UBP-302 (24[3-[(25)-2-amino-2-carboxyethy1]-2,6-dioxo-3,6-dihydropyrimidin 1(2H)-yllmethyl)benzoic acid) may hamper Hcy-dependent platelet aggregation. All the tested compounds significantly inhibited Hcy-augmented aggregation of blood platelets stimulated either with arachidonate or collagen. Hcy stimulated the generation of superoxide anion in whole blood samples in a concentration-dependent manner; however, this process appeared as independent on ionotropic glutamate receptors, as well as on NADPH oxidase and protein kinase C, and was not apparently associated with the extent of either arachidonate- or collagen-dependent platelet aggregation. Moreover, Hcy acted as a significant fluidizer of surface (more hydrophilic) and inner (more hydrophobic) regions of platelet membrane lipid bilayer, when used at the concentration range from 10 to 50 mu mol/l. However, this effect was independent on the Hcy action through glutamate ionotropic receptors, since there was no effects of MK-801, CNQX or UBP-302 on Hcy-mediated membrane fluidization. In conclusion, Hcy-induced changes in whole blood platelet aggregation are mediated through the ionotopic excitotoxic receptors, although the detailed mechanisms underlying such interactions remain to be elucidated.
机译：同型半胱氨酸（Hcy）是一种兴奋性毒性氨基酸。通过拮抗谷氨酰胺受体，有可能预防同型半胱氨酸引起的毒性，包括止血损伤。使用花生四烯酸和胶原作为血小板激动剂的阻抗聚集测定法，我们测试了血小板NMDA（N-甲基-D-天冬氨酸）、AMPA（a-氨基-3-羟基-5-甲基-4-异恶唑丙酸）和红藻氨酸受体及其抑制剂MK-801（马来酸氢二唑西平[5R，10514-1-1-5-甲基-10,11-二氢-5Hdibenzo（a，D]环庚烷-5,10-亚胺），CNQX（7-硝基-2,3-二氧基-1,4-二氢喹啉-6碳三烯）和UBP-302（24[3-[（25）-2-氨基-2-羧乙基]-2,6-二氧基-3,6-二氢嘧啶-1（2H）-甲基）苯甲酸）可能会阻碍Hcy依赖性血小板聚集。所有受试化合物均能显著抑制花生四烯酸或胶原蛋白刺激的同型半胱氨酸增强的血小板聚集。同型半胱氨酸以浓度依赖的方式刺激全血中超氧阴离子的产生；然而，这一过程似乎独立于离子型谷氨酸受体，以及NADPH氧化酶和蛋白激酶C，与花生四烯酸或胶原依赖性血小板聚集的程度没有明显的相关性。此外，当浓度在10至50μmol/l范围内使用时，同型半胱氨酸作为血小板膜脂质双层表面（更亲水）和内部（更疏水）区域的重要流态化剂。然而，这种作用通过谷氨酸离子受体独立于同型半胱氨酸的作用，因为MK-801、CNQX或UBP-302对同型半胱氨酸介导的膜流态化没有影响。总之，同型半胱氨酸诱导的全血血小板聚集的变化是通过离子受体介导的，尽管这种相互作用的详细机制仍有待阐明。

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