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Flow Cytometry Analysis of Immune Cells Within Murine Aortas
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单克隆抗CD18抗体在体外和体内阻止氨酸白血的细胞间生物合成,并防止白血依赖的冠状动脉血管抵抗和心肌硬度的增加.

A Sala1, G Rossoni, F Berti

  • 1Center for Cardiopulmonary Pharmacology, University of Milan, Italy.

Circulation
|March 29, 2000
PubMed
概括

PMNL-内皮细胞的粘附促进了氨酸白血 (cys-LT) 的形成,有助于心肌硬化. 通过抗体阻断CD18粘附分子,可以降低心肌梗塞期间的cys-LT合成和冠状动脉抵抗.

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科学领域:

  • 免疫学 免疫学 免疫学
  • 心血管生理学心血管生理学
  • 生物化学 生物化学

背景情况:

  • 乙氨基白血 (cys-LT) 是强大的调解剂,可以收缩血管并增加血管的通透性.
  • 囊-LT的跨细胞合成涉及多态核白细胞 (PMNL) 和内皮细胞之间的合作.
  • 假设PMNL-内皮细胞粘附是启动血管活性cys-LT形成的关键步骤.

研究的目的:

  • 研究PMNL-内皮细胞粘附在cys-LT合成中的作用.
  • 为了确定是否阻断β-2-整合素的CD18亚单元可以抑制cys-LT的形成和相关的心血管影响.

主要方法:

  • 研究了抗CD18单克隆抗体对cys-LT合成在体外子心脏模型和体内冠状动脉绑定子模型中的作用.
  • 施用甲基甲或A-23187来挑战PMNL透的心脏.
  • 测量了 cys-LT 合成,冠状动脉 perfusion 压力,PMNL 透 (髓氧化酶活性) 和尿路白血素 E (((4) 排泄.

主要成果:

  • 对抗CD18抗体的预处理防止了cys-LT的合成,并在应对挑战时增加了冠状动脉输液压.
  • 抗体减少了PMNL透到心脏中的情况.
  • 在体内,抗CD18抗体的施用抑制了冠状动脉结合后尿路中白血E(4) 排泄的增加,这表明5-氧化酶通路的激活减少.

结论:

  • 通过CD18介导的PMNL内皮细胞粘附,对于cys-LT形成至关重要.
  • 抑制这种粘附途径减少了 cys-LT 的产生,并可能减轻急性心肌梗塞期间心肌硬度和冠状动脉阻力增加.