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阿尔法-托科菲罗尔通过蛋白激酶C依赖机制抑制人体血小板的聚合
J E Freedman1, J H Farhat, J Loscalzo
1Whitaker Cardiovascular Institute, Boston University School of Medicine, MA 02118-2394, USA.
Circulation
|November 15, 1996
概括
维生素E (alpha-tocopherol) 通过融入血小板,抑制血小板聚合. 这种涉及蛋白激酶C (PKC) 的机制可能解释了其对心血管的好处.
科学领域:
- 生物化学 生物化学
- 心血管研究研究心血管研究
- 营养科学 营养科学
背景情况:
- 流行病学研究表明,维生素E (alpha-tocopherol) 对心血管健康有好处,可能是通过对LDL的抗氧化作用.
- 已知维生素E在体外抑制血小板聚合和粘附,但潜在的机制尚不清楚.
研究的目的:
- 为了研究α-托科菲罗尔抑制血小板聚合的机制.
- 确定阿尔法-托科菲罗尔对血小板聚合的影响是否与其纳入血小板和蛋白激酶C (PKC) 活性有关.
主要方法:
- 富于血小板的血被用α-托科菲罗尔或对照抗氧化剂治疗.
- 测量了对各种激动剂 (ADP,酸,PMA) 的血小板聚合敏感性.
- 蛋白激酶C (PKC) 活性通过测量其47kD基质的酸化来评估.
- 人体受试者接受了口服的α-托哥菲罗尔补充剂,并分析了血小板α-托哥菲罗尔含量和聚合.
主要成果:
- 阿尔法-托科菲罗尔被纳入血小板与降低血小板聚合相关 (r = -0.78).
- 血小板对聚合激动剂的敏感性在阿尔法托科菲罗尔治疗后显著下降.
- 阿尔法托科菲罗尔抑制的博 (PMA) 诱导的蛋白激酶C (PKC) 刺激.
- 口服补充剂增加了血小板α-托科菲罗尔,并抑制了人类的PMA介导的聚合和PKC活性.
结论:
- 通过PKC依赖的途径,阿尔法-托科菲罗尔的血小板内置抑制了聚合.
- 这种机制可能有助于在流行病学研究中观察到的alpha-tocopherol的心脏保护作用.
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