由脂聚糖胺诱导的全身炎症增加了子在气球和支架损伤后的neointimal形成
Haim D Danenberg1, Frederick G P Welt, Matthew Walker
1Harvard-MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. danen@mit.edu
Circulation
|June 19, 2002
概括
在动脉损伤期间非特异性免疫系统刺激会恶化新极度增生和复原. 这表明,炎症在这些血管疾病的发展中起着关键作用.
科学领域:
- 血管生物学 血管生物学
- 免疫学 免疫学 免疫学
- 心血管研究的心血管研究.
背景情况:
- 动脉损伤后的炎症反应与新极端增生和复原相关.
- 天生的免疫系统刺激可能会影响血管损伤的结果.
研究的目的:
- 调查先天免疫系统刺激是否会影响机械动脉损伤后的结果.
- 检查脂多糖 (LPS) 在调节新极度增生症中的作用.
主要方法:
- 子经历了下动脉气球损伤,并接受了脂聚糖化物 (LPS) 注射.
- 测量了系统性炎症标志物 (白蛋白-1β) 和单细胞激活 (CD14).
- 在受伤后评估了巨细胞透,光线狭窄以及新密与中密的比率.
主要成果:
- 使用LPS增加了全身炎症和单细胞CD14表达.
- 用LPS治疗的子显示显著增加了巨细胞透和新极度增生.
- 在接受LPS治疗的动物中,光线狭窄和新近距离与中间距离的比率显著更高,这种效应被抗CD14抗体消除了.
结论:
- 同时的先天性免疫刺激和动脉损伤加剧了新极限的形成.
- 与炎症相关的疾病可能会增加血管形成术后复原症的风险.
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