Do platelet apoptosis, activation, aggregation, lipid peroxidation and platelet-leukocyte aggregate formation occur simultaneously in hyperlipidemia?
Do platelet apoptosis, activation, aggregation, lipid peroxidation and platelet-leukocyte aggregate formation occur simultaneously in hyperlipidemia?
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DOI：
10.1016/j.clinbiochem.2005.09.005
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发表时间：
2005-12-01
影响因子：
2.8
通讯作者：
Yardimci, KT
中科院分区：
文献类型：
--
作者：
Sener, A;Ozsavci, D;Yardimci, KT
目的：高胆固醇血症患者循环脂蛋白可引起血小板组成和功能异常。本研究旨在探讨高脂血症患者血小板凋亡、血小板活化、血小板聚集、血小板-白细胞聚集（PLA）形成和脂质过氧化是否同时发生。设计与方法：采用流式细胞术检测8例高脂血症患者和8例正常人的GpIIb/IIIa （CD41a）、p -选择素（CD62-P）、血小板结合纤维蛋白原（抗纤维蛋白原）、血小板膜磷脂酰基丝氨酸（PS）、血小板-单核细胞聚集体（single - pla）和血小板-中性粒细胞聚集体（neut-PLA）的表达。ADP （10 μ M）活化血小板。此外，测定ADP诱导的血小板聚集反应、血小板丙二醛（MDA）和谷胱甘肽（GSH）水平。结果：血小板激活前，高脂血症患者血小板CD62-P、抗纤维蛋白原、膜联蛋白v、单聚乳酸、中性聚乳酸、血小板MDA水平及血小板聚集反应均显著高于对照组（P < 0.01, P < 0.01, P < 0.01, P < 0.001, P < 0.001, P < 0.01, P < 0.001），而GpIIb/IIIa表达及GSH水平差异无统计学意义（P < 0.05）。对照组ADP激活后CD62-P、抗纤维蛋白原、膜联蛋白v水平均显著升高（P < 0.05、P < 0.05、P < 0.01）。在高脂血症患者中，激活后annexin-V的表达显著增加（P < 0.01），而GpIIb/ IIIa、CD62-P和抗纤维蛋白原的表达保持不变（P < 0.05）。发现患者总胆固醇（T-CHO）、低密度脂蛋白胆固醇（LDL-C）、血清纤维蛋白原（S-FGN）和高密度脂蛋白胆固醇（HDL-C）水平与血小板CD62-P、抗纤维蛋白原、膜联蛋白v、单聚乳酸和丙二醛水平相关。结论：总之，在高脂血症中，一些血小板在循环中处于活化状态，脂质过氧化增加、早期凋亡、血小板-白细胞聚集形成和血小板聚集共同伴随这一过程。(C) 2005加拿大临床化学学会。版权所有。
Objectives: The circulating lipoproteins may cause some abnormalities in platelet composition and function in hypercholesterolemia. The aim Of this Study was to investigate whether platelet apoptosis, platelet activation, platelet aggregation, platelet-leukocyte aggregate (PLA) formation and lipid peroxidation occur simultaneously in hyperlipidemia.Design and methods: Expression of GpIIb/IIIa (CD41a), P-selectin (CD62-P), platelet-bound fibrinogen (antifibrinogen), platelet membrane phosphatidylserine (PS), platelet-monocyte aggregates (mono-PLA) and platelet-neutrophil aggregates (neut-PLA) was measured in eight hyperlipidemic and eight normal subjects using flow cytometry. ADP (10 mu M) was used to activate platelets. Furthermore, ADP induced platelet aggregation responses, platelet malondialdehyde (MDA) and glutathione (GSH) levels were determined.Results: Before platelet activation, platelet CD62-P, anti Fibrinogen, annexin-V, mono-PLA, neut-PLA and platelet MDA levels as well as platelet aggregation responses in the hyperlipidemics were significantly higher than those in the controls (P < 0.01, P < 0.01, P < 0.01, P < 0.001, P < 0.001, P < 0.01, P < 0.001, respectively), whereas GpIIb/IIIa expression and GSH levels were not different significantly (P > 0.05). In the control group, CD62-P, antifibrinogen and annexin-V levels increased significantly after ADP activation (P < 0.05, P < 0.05, P < 0.01, respectively). In hyperlipidemic Subjects, annexin-V expression increased significantly after activation (P < 0.01), whereas expression of GpIIb/ IIIa, CD62-P and anti fibrinogen remained unchanged (P > 0.05). The levels of total cholesterol (T-CHO), low density lipoprotein cholesterol (LDL-C), serum fibrinogen (S-FGN) and high density lipoprotein cholesterol (HDL-C) in patients were found to be correlated with platelet CD62-P, anti Fibrinogen, annexin-V, mono-PLA and MDA.Conclusions: In conclusion, it seems that in hyperlipidemia, some platelets are in an activated state in circulation, and that increased lipid peroxidation, early apoptosis, platelet-leukocytes aggregate formation and platelet aggregation altogether accompany this process. (C) 2005 The Canadian Society of Clinical Chemists. All rights reserved.