牛磺酸和咖啡因对血小板活性和止血功能的协同作用

A. Santhakumar, Nicolette Fozzard, A. Perkins, I. Singh
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引用次数: 12

摘要

几项研究表明,含有牛磺酸和咖啡因的能量饮料对心脏健康有害。本研究旨在研究牛磺酸和咖啡因对血小板和止血的协同作用,因为血小板过度活跃是已知的心血管疾病的预测因子。12名年龄在18 - 60岁之间的健康志愿者的血液分别或同时加入500µm牛磺酸和700µm咖啡因。采用ADP和胶原诱导的血小板聚集试验评估血小板活性,并通过凝血谱测试、血糖、脂质谱和炎症标志物C反应蛋白评估(CRP)评估止血功能。确定了牛磺酸和咖啡因在体外抑制血小板过度活跃所需的最佳时间和剂量。低剂量牛磺酸和咖啡因(T+C)对ADP和胶原诱导的血小板聚集的抑制作用优于牛磺酸和咖啡因(p < 0.05)。牛磺酸和T+C可显著提高凝血酶原凝血时间(p < 0.05),而单独使用咖啡因可显著降低凝血酶原凝血时间(p < 0.05)。单独使用咖啡因可使CRP升高(p < 0.05)。唇形参数未见明显变化。这些数据支持了我们的假设,即低浓度的牛磺酸和咖啡因协同作用,在能量饮料中发现浓度更高,可能有助于降低血小板活性和延长凝块形态。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Synergistic Effect of Taurine and Caffeine on Platelet Activity and Hemostatic Function
Several studies have shown the deleterious effects of energy drinks, containing taurine and caffeine, on cardiac health. This study aimed to examine synergistic effect of taurine and caffeine on p latelets and haemostasis because platelet hyperactivity is a known predictor of cardiovascular diseases. Blood fro m t welve healthy volunteers aged 18 - 60 years was incubated with 500 µM taurine and 700 µM caffeine indiv idually or together. Platelet activity was evaluated using platelet aggregation assays induced by ADP and collagen, and, haemostatic function by coagulation profile testing, glucose, lipid profile and inflammat ion marker C- reactive protein assessment (CRP). The optimal time and doses of taurine and caffeine required to inhib it platelet hyperactivity in vitro were established. A comb ined action of lower doses of taurine and caffeine (T+C) inhibited platelet aggregation, induced by ADP and collagen, greater than taurine or caffeine individually (p < 0.05). Taurine and T+C increased prothrombin clotting time (PT) significantly (p < 0.05), wh ile caffeine alone decreased PT (p < 0.05). Caffeine alone increased CRP (p < 0.05). No significant change was observed in lip id parameters. These data support our hypothesis that, synergistically lower concentrations of taurine and caffeine, found in much h igher concentrations in energy drinks, may be instrumental in reducing platelet activ ity and prolongation of clot format ion.
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