格林抑制了人类内皮细胞中的炎症反应和核因子-kappaB激活
Wei Gen Li1, Dan Gavrila, Xuebo Liu
1Department of Internal Medicine, Cardiovascular Division, University of Iowa College of Medicine, Iowa City, IA 52242, USA.
Circulation
|May 1, 2004
概括
格雷林是一种类激素,通过抑制内皮细胞的炎症性细胞因子产生和细胞粘附来表现出新的抗炎作用. 这些研究结果表明,格林林.
科学领域:
- 内分泌学 在内分泌学.
- 免疫学 免疫学 免疫学
- 血管生物学 血管生物学
背景情况:
- 格雷林是一种生长激素释放的,已知在缓冲症和败血症休克中具有有益作用.
- 由细胞因子驱动的炎症是这些疾病的核心.
- 增长激素分泌受体存在于血管中,这表明格林在血管炎症中的作用.
研究的目的:
- 在人体内皮细胞中研究格林的抗炎潜力.
- 评估格林对内毒素诱导的炎症的作用 in vivo 在老鼠身上.
主要方法:
- 人类静脉内皮细胞 (HUVECs) 用瘤缩因子-α (TNF-α) 进行刺激.
- 测量了细胞因子释放,单核细胞粘附和核因子-kappaB (NF-kappaB) 激活.
- 在老鼠中,静脉注射了内毒素和 ghrelin.
主要成果:
- 格林在HUVEC中显著抑制了基底和TNF-α诱导的细胞因子释放和单核细胞结合.
- 格林在老鼠中抑制了内毒素诱导的细胞因子产生.
- 该阻断了氧化还原介导信号传递,并抑制了NF-kappaB的激活.
- 德-乙格林缺乏这些抗炎作用,表明受体依赖作用.
结论:
- 格林在内皮细胞中表现出强大的抗炎性质,无论是体外还是体外.
- 这些作用包括抑制细胞因子产生,细胞粘附和NF-kappaB激活.
- 格林可能在调节诸如动脉样硬化等炎症性疾病中发挥作用,特别是在格林水平降低的情况下.
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