阿波利波蛋白C-I在阿波利波蛋白E-Knockout小鼠中对脂多糖糖诱导的动脉样硬化发展起着至关重要的作用
Marit Westerterp1, Jimmy F P Berbée, Nuno M M Pires
1The Netherlands Organization for Applied Scientific Research-Quality of Life, Department of Biomedical Research, Gaubius Laboratory, Leiden, The Netherlands. M.Westerterp@lumc.nl
Circulation
|October 31, 2007
概括
脂蛋白C-I (apoCI) 通过放大炎症反应,加剧了脂聚糖 (LPS) 诱导的动脉样硬化. 这表明apoCI血水平可能会在慢性感染中加速动脉样硬化.
科学领域:
- 心血管研究研究心血管研究
- 免疫学 免疫学 免疫学
- 动脉样硬化研究 动脉样硬化研究
背景情况:
- 来自グラム阴性细菌的脂聚糖 (LPS) 通过炎症促进动脉样硬化.
- 已知Apolipoprotein C-I (apoCI) 在体外和体内增强LPS诱导的炎症.
研究的目的:
- 调查内源性apoCI在小鼠LPS诱导动脉样硬化发展中的作用.
主要方法:
- 缺乏阿波蛋白E的小鼠,有或没有apoCI表达,在10周内给予LPS或载体.
- 动脉样硬化在大动脉根部得到量化.
- 评估了纤维素素和E-选择素的血水平,以及巨细胞炎症性细胞因子的产生.
主要成果:
- 在apoe-/- apoc1+/+小鼠中,LPS的使用增加了动脉样损伤面积的60%,但在apoe-/- apoc1-/-小鼠中没有增加.
- apoCI表达增加了LPS诱导的血纤维素和E-选择素水平.
- 巨细胞衍生和高脂相关的apoCI都增强了巨细胞的LPS诱导的TNF-alpha产生.
结论:
- 内源性apoCI在apoe-/-小鼠中极大地促进LPS诱导的动脉样硬化,主要是通过增强的炎症反应.
- 升高的apoCI血水平可能导致慢性感染中的动脉样硬化加速.
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