背景:甘油溶血磷脂(甘油-LPLs),已知它们能发挥强大的生物活性,已被证明在体外从活化的血小板分泌;然而,它们与体内血小板活化的关系尚未阐明.在这项研究中,我们调查了每种甘油-LPL和血清素的血液水平之间的相关性,血小板活化的生物标志物,在人类受试者中阐明体内甘油-LPL中血小板活化的参与。
结果:我们测量了141例连续接受冠状动脉造影的患者的血浆5-羟色胺水平(急性冠状动脉综合征,n=38;稳定型心绞痛,n=71;血管造影正常的冠状动脉,n=32),并研究了血浆5-羟色胺水平与甘油-LPLs之间的相关性。结果表明,血浆5-羟色胺和血浆溶血磷脂酰丝氨酸(LysoPS)水平之间存在特定且显着的关联。相反,常规阿司匹林摄入未能影响血浆LysoPS水平,尽管事实上血浆溶血磷脂酸,溶血磷脂酰乙醇胺,溶血磷脂酰甘油,定期服用阿司匹林的患者溶血磷脂酰肌醇水平较低。
结论:我们发现血液中5-羟色胺水平和Lysops之间存在特定的正相关性,一种新的脂质介质。因此,LysoPS可能特异性参与强血小板活化,这与血清素的释放有关。
结论:我们目前的研究结果表明,LysoPS可能参与动脉粥样硬化疾病的发病机制。
BACKGROUND: Glycero-lysophospholipids (glycero-LPLs), which are known to exert potent biological activities, have been demonstrated to be secreted from activated platelets in vitro; however, their association with platelet activation in vivo has not been yet elucidated. In this study, we investigated the correlations between the blood levels of each glycero-LPL and serotonin, a biomarker of platelet activation, in human subjects to elucidate the involvement of platelet activation in glycero-LPLs in vivo.
RESULTS: We measured the plasma serotonin levels in 141 consecutive patients undergoing coronary angiography (acute coronary syndrome, n = 38; stable angina pectoris, n = 71; angiographically normal coronary arteries, n = 32) and investigated the correlations between the plasma levels of serotonin and glycero-LPLs. The results revealed the existence of a specific and significant association between the plasma serotonin and plasma lysophosphatidylserine (LysoPS) levels. On the contrary, regular aspirin intake failed to affect the plasma LysoPS levels despite the fact that the plasma lysophosphatidic acid, lysophosphatidylethanolamine, lysophosphatidylglycerol, and lysophosphatidylinositol levels were lower in those who had taken aspirin regularly.
CONCLUSIONS: We found a specific positive correlation between the blood levels of serotonin and LysoPS, a new lipid mediator. Thus, LysoPS might be specifically involved in strong platelet activation, which is associated with the release of serotonin.
CONCLUSIONS: Our present results suggest the possible involvement of LysoPS in the pathogenesis of atherosclerotic diseases.