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铁依赖的人类血小板激活和基形成:涉及蛋白质激酶C
D Praticó1, M Pasin, O P Barry
1Institute of Clinical Medicine I, University La Sapienza, the National Institute of Nutrition, Rome, Italy.
Circulation
|June 22, 1999
概括
铁直接激活人体血小板,导致聚合和血栓素形成. 这个过程涉及基 (OH.) 产生和蛋白激酶C (PKC) 信号,有助于动脉样硬化风险.
科学领域:
- 生物化学 生物化学
- 血液学 血液学 血液学
- 心血管研究研究心血管研究
背景情况:
- 铁调节脂质过氧化,并与动脉样硬化的进展有关.
- 释放的铁在调节血细胞成分,特别是血小板中的作用尚不清楚.
研究的目的:
- 为了研究铁,氧自由基的形成和血小板功能之间的联系.
- 为了确定铁是否直接影响血小板反应.
主要方法:
- 由原刺激的全血聚合测定.
- 基 (OH.) 的测量 使用二基酸盐的形成.
- 评估血小板聚合,血栓素B2 (TxB2) 形成和蛋白质激酶C (PKC) 转位.
- 使用铁化剂 (德菲洛克萨),激素清除剂 (catalase,曼尼托尔,脱氧) 和PKC抑制剂 (GF 109203X).
主要成果:
- 原诱导了血小板聚合,TxB2的形成和OH的增加. 一个层次,一个层次.
- 德费罗胺和酶抑制了由原诱导的聚合.
- 铁 (Fe2+) 剂量取决于诱导的血小板聚合,TxB2形成和PKC转位.
- 铁诱导的血小板激活伴随着OH的增加. 水平,这些水平被曼尼托和脱氧降低了.
- 抑制PKC可以防止依赖铁的血小板聚合,但不能阻止OH. 在生产,生产,生产.
结论:
- 铁直接与人体血小板相互作用并激活它们.
- 铁介导的血小板激活涉及基 (OH.) 蛋白酶C (PKC) 的形成和信号传递.
- 这些发现阐明了铁过载可能促进动脉样硬化和冠状动脉疾病的机制.
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