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循环氧化原酶异型和血小板血管壁相互作用在阿波利波蛋白E淘汰赛小鼠模型的动脉样硬化

Orina A Belton¹, Angela Duffy, Sinead Toomey

¹Department of Clinical Pharmacology and Institute of Biopharmaceutical Sciences, Royal College of Surgeons in Ireland 123, St Stephens Green, Dublin 2, Ireland. obelton@rcsi.ie

|November 26, 2003

概括

环氧化原酶-1 (COX-1) 在预防动脉样硬化早期病变形成方面至关重要. 抑制COX-1减少了病变的发展,而抑制COX-2对动脉样硬化进展或血小板活性没有影响.

科学领域:

心血管研究研究心血管研究
炎症和免疫学炎症和免疫学
药理学药理学是指药理学的学科.

背景情况:

在人类动脉样硬化中,循环氧化酶 (COX) 活性升高.
COX产品可能会影响疾病进展和血小板功能.
在动脉样硬化中COX-1和COX-2的作用需要进一步阐明.

研究的目的:

研究COX-1和COX-2在血小板血管壁相互作用中的特定作用.
在小鼠模型中确定选择性COX抑制对动脉样硬化发展的影响.

主要方法:

在高胆固醇饮食中缺乏阿波利波蛋白E (apoE-/-) 的小鼠接受了选择性COX-1或COX-2抑制剂的治疗.
测量了尿中的前环素和血栓素代谢物.
对血管病变进行了COX异型表达,血小板标记 (CD41),巨细胞标记 (CD68) 和细胞死亡蛋白 (Bax) 的分析.

主要成果:

在apoE-/-小鼠的血管病变中,COX-1和COX-2都被诱导.
选择性COX-2抑制没有影响病变形成或血小板活性.
选择性COX-1抑制减少了血栓素生成和病变的发展,但血小板沉积仍然存在.

结论:

在这种动脉样硬化模型中,COX-1在病变发展的早期阶段起着重要作用.
抑制COX-1似乎可以防止严重的病变形成,尽管血管损伤正在进行中.
抑制COX-2对病变的发展或血小板血管壁相互作用没有明显的影响.

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