氧化脂蛋白降解了内皮表面层:对血小板内皮细胞粘附的影响
H Vink1, A A Constantinescu, J A Spaan
1Department of Medical Physics, University of Amsterdam, Amsterdam, The Netherlands. h.vink@amc.uva.nl
Circulation
|April 4, 2000
概括
氧化低密度脂蛋白 (Ox-LDL) 破坏了内皮表面层,增加了血管壁的粘性. 这种效应由由氧衍生的自由基介导,可以被抗氧化剂阻断.
科学领域:
- 心血管生物学 心血管生物学
- 内皮细胞功能 内皮细胞功能
- 动脉样硬化研究 动脉样硬化研究
背景情况:
- 内皮表面层 (ESL) 在流动的血细胞和内皮细胞 (EC) 表面之间保持隔离.
- 氧化低密度脂蛋白 (Ox-LDL) 参与了动脉生成.
- 需要阐明Ox-LDL在ESL破坏和血管粘合性中的作用.
研究的目的:
- 调查Ox-LDL破坏ESL的假设,导致血管壁粘性增加.
- 确定由氧衍生自由基在Ox-LDL诱导的ESL变化中的作用.
主要方法:
- 肠道显微镜被用来观察红细胞-EC表面距离在仓鼠的肌肉.
- 氧-LDL是由CuSO(4) 氧化原生LDL而制备的.
- 评估了Ox-LDL和抗氧化剂 (超氧化解酶和酶) 对ESL尺寸和血小板-EC粘附的影响.
主要成果:
- 在25分钟内,Ox-LDL暂时将ESL维度减少了60%.
- 这种ESL减少与血小板-EC粘附的短暂增加相关.
- 综合使用超氧化物转化酶和转化酶完全阻断了Ox-LDL对ESL和血小板粘附的影响.
结论:
- 来自氧的自由基调解了由Ox-LDL破坏内皮表面层的过程.
- 通过Ox-LDL破坏ESL有助于增加血管壁粘性.
- 抗氧化剂治疗可以防止Ox-LDL诱导的ESL变化和相关的血小板粘附.
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