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.

Findings

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).

Interpretation

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.

中文翻译：

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花青素补充剂对血脂异常患者血小板功能的剂量依赖性影响：一项随机临床试验

背景

血脂异常诱导血小板过度活化和过度聚集，这与血栓形成有关。花青素可在体外和高脂饮食小鼠体内抑制血小板功能，但其对血脂异常受试者血小板功能的影响仍不清楚。本研究旨在探讨不同剂量花青素对血脂异常个体血小板功能的影响。

方法

进行了一项双盲、随机、对照试验。最初被诊断患有血脂异常的 93 名个体被随机分配到安慰剂组或 40、80、160 或 320 毫克/天花青素组。补充剂是花青素胶囊（Medox，挪威）。在基线、6周和12周时，通过光聚集法检测富血小板血浆的血小板聚集、P-选择素、活化的GPⅡbⅢa、活性氧（ROS）和线粒体膜电位。

发现

与安慰剂组相比，花青素 80 mg/d 持续 12 周可减少胶原诱导的血小板聚集（-3.39±2.36%）和活化 GPⅡbⅢa（-8.25±2.45%）（P  < 0.05）。此外，与安慰剂组相比，320 mg/天的花青素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%）、血小板活性氧水平（-14.55±1.86%） , 和线粒体膜电位 (7.40±1.56%) ( P  < 0.05)。花青素与血小板聚集衰减、线粒体膜电位和 ROS 水平呈剂量反应关系（P对于趋势 <0.05)。此外，12周干预后，血脂异常受试者胶原诱导（r = 0.473）或ADP诱导（r = 0.551）血小板聚集的变化与活性氧水平呈显着正相关（P  < 0.05）。

解释

花青素补充剂剂量依赖性地减弱血小板功能，12 周补充 80 毫克/天或更多的花青素可降低血脂异常个体的血小板功能。