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Abstract：
BACKGROUND: Dyslipidemia induces platelet hyperactivation and hyper-aggregation, which are linked to thrombosis. Anthocyanins could inhibit platelet function in vitro and in mice fed high-fat diets with their effects on platelet function in subjects with dyslipidemia remained unknown. This study aimed to investigate the effects of different doses of anthocyanins on platelet function in individuals with dyslipidemia.
METHODS: A double-blind, randomized, controlled trial was conducted. Ninety-three individuals who were initially diagnosed with dyslipidemia were randomly assigned to placebo or 40, 80, 160 or 320 mg/day anthocyanin groups. The supplementations were anthocyanin capsules (Medox, Norway). Platelet aggregation by light aggregometry of platelet-rich plasma, P-selectin, activated GPⅡbⅢa, reactive oxygen species (ROS), and mitochondrial membrane potential were tested at baseline, 6 weeks and 12 weeks.
RESULTS: Compared to placebo group, anthocyanins at 80 mg/day for 12 weeks reduced collagen-induced platelet aggregation (-3.39±2.36%) and activated GPⅡbⅢa (-8.25±2.45%) (P < 0.05). Moreover, compared to placebo group, anthocyanins at 320 mg/day inhibited collagen-induced platelet aggregation (-7.05±2.38%), ADP-induced platelet aggregation (-7.14±2.00%), platelet ROS levels (-14.55±1.86%), and mitochondrial membrane potential (7.40±1.56%) (P < 0.05). There were dose-response relationships between anthocyanins and the attenuation of platelet aggregation, mitochondrial membrane potential and ROS levels (P for trend <0.05). Furthermore, significantly positive correlations were observed between changes in collagen-induced (r = 0.473) or ADP-induced (r = 0.551) platelet aggregation and ROS levels in subjects with dyslipidemia after the 12-week intervention (P < 0.05).
CONCLUSIONS: Anthocyanin supplementation dose-dependently attenuates platelet function, and 12-week supplementation with 80 mg/day or more of anthocyanins can reduce platelet function in individuals with dyslipidemia.
BACKGROUND: None.
METHODS: A double-blind, randomized, controlled trial was conducted. Ninety-three individuals who were initially diagnosed with dyslipidemia were randomly assigned to placebo or 40, 80, 160 or 320 mg/day anthocyanin groups. The supplementations were anthocyanin capsules (Medox, Norway). Platelet aggregation by light aggregometry of platelet-rich plasma, P-selectin, activated GPⅡbⅢa, reactive oxygen species (ROS), and mitochondrial membrane potential were tested at baseline, 6 weeks and 12 weeks.
RESULTS: Compared to placebo group, anthocyanins at 80 mg/day for 12 weeks reduced collagen-induced platelet aggregation (-3.39±2.36%) and activated GPⅡbⅢa (-8.25±2.45%) (P < 0.05). Moreover, compared to placebo group, anthocyanins at 320 mg/day inhibited collagen-induced platelet aggregation (-7.05±2.38%), ADP-induced platelet aggregation (-7.14±2.00%), platelet ROS levels (-14.55±1.86%), and mitochondrial membrane potential (7.40±1.56%) (P < 0.05). There were dose-response relationships between anthocyanins and the attenuation of platelet aggregation, mitochondrial membrane potential and ROS levels (P for trend <0.05). Furthermore, significantly positive correlations were observed between changes in collagen-induced (r = 0.473) or ADP-induced (r = 0.551) platelet aggregation and ROS levels in subjects with dyslipidemia after the 12-week intervention (P < 0.05).
CONCLUSIONS: Anthocyanin supplementation dose-dependently attenuates platelet function, and 12-week supplementation with 80 mg/day or more of anthocyanins can reduce platelet function in individuals with dyslipidemia.
BACKGROUND: None.
摘要：
背景：血脂异常诱导血小板过度活化和过度聚集，与血栓形成有关。花青素可以在体外和高脂饮食的小鼠中抑制血小板功能，其对血脂异常受试者血小板功能的影响尚不清楚。本研究旨在探讨不同剂量花青素对血脂异常患者血小板功能的影响。
方法：双盲，随机化，进行了对照试验。最初被诊断为血脂异常的93人被随机分配到安慰剂组或40、80、160或320mg/天的花青素组。补充剂是花色苷胶囊(Medox，挪威)。通过富血小板血浆的光聚集法测量血小板聚集，P-选择素,激活的GPⅡbⅢa,活性氧（ROS），和线粒体膜电位在基线测试，6周和12周。
结果：与安慰剂组相比，花色苷在80mg/d下连续12周降低了胶原诱导的血小板聚集（-3.39±2.36％），并激活了GPⅡbⅢa（-8.25±2.45％）（P<0.05）。此外，与安慰剂组相比，320毫克/天的花色苷抑制胶原蛋白诱导的血小板聚集（-7.05±2.38％），ADP诱导的血小板聚集（-7.14±2.00%），血小板ROS水平（-14.55±1.86%），线粒体膜电位(7.40±1.56%)(P<0.05)。花青素与血小板聚集的衰减之间存在剂量-反应关系，线粒体膜电位和ROS水平(P<0.05)。此外，干预12周后,血脂异常患者胶原诱导(r=0.473)或ADP诱导(r=0.551)血小板聚集变化与ROS水平呈正相关(P<0.05)。
结论：补充花青素剂量依赖性地减弱血小板功能，12周补充80毫克/天或更多的花色苷可降低血脂异常个体的血小板功能。
背景：无。
方法：双盲，随机化，进行了对照试验。最初被诊断为血脂异常的93人被随机分配到安慰剂组或40、80、160或320mg/天的花青素组。补充剂是花色苷胶囊(Medox，挪威)。通过富血小板血浆的光聚集法测量血小板聚集，P-选择素,激活的GPⅡbⅢa,活性氧（ROS），和线粒体膜电位在基线测试，6周和12周。
结果：与安慰剂组相比，花色苷在80mg/d下连续12周降低了胶原诱导的血小板聚集（-3.39±2.36％），并激活了GPⅡbⅢa（-8.25±2.45％）（P<0.05）。此外，与安慰剂组相比，320毫克/天的花色苷抑制胶原蛋白诱导的血小板聚集（-7.05±2.38％），ADP诱导的血小板聚集（-7.14±2.00%），血小板ROS水平（-14.55±1.86%），线粒体膜电位(7.40±1.56%)(P<0.05)。花青素与血小板聚集的衰减之间存在剂量-反应关系，线粒体膜电位和ROS水平(P<0.05)。此外，干预12周后,血脂异常患者胶原诱导(r=0.473)或ADP诱导(r=0.551)血小板聚集变化与ROS水平呈正相关(P<0.05)。
结论：补充花青素剂量依赖性地减弱血小板功能，12周补充80毫克/天或更多的花色苷可降低血脂异常个体的血小板功能。
背景：无。
