雌激素调节受损动脉中的炎症媒介表达和中性粒细胞化学反应
Andrew P Miller1, Wenguang Feng, Dongqi Xing
1Vascular Biology and Hypertension Program, University of Alabama at Birmingham, 1047 Zeigler Research Bldg, 703 19th St S, Birmingham, AL 35294-0007, USA. apmiller@uab.edu
Circulation
|September 9, 2004
概括
雌激素 (E2) 通过减少关键炎症分子和中性粒细胞吸引力,显著减少受伤后的早期血管炎症. 这种激素治疗有助于减轻身体对动脉损伤的反应.
科学领域:
- 血管生物学 血管生物学
- 内分泌学 在内分泌学.
- 炎症研究 炎症研究
背景情况:
- 雌激素 (17β-雌激醇;E2) 曾经被证实可以抑制受伤后大鼠动脉中新心形成和白细胞迁移.
- 这项研究调查了E2在气球血管造形术后调节早期炎症媒介表达中的作用.
研究的目的:
- 为了测试E2是否抑制粘附分子,化学因子和细胞因子在鼠尾动脉的表达,在气球损伤后的早期.
- 要确定E2是否减弱白细胞的进入,并调节血管损伤反应.
主要方法:
- 经过卵巢切除的老鼠接受了E2或车载,其次是心脏动脉的气球损伤.
- 基因表达 (RT-PCR),蛋白质水平 (ELISA) 和中性粒细胞化学反应在受伤后的2,6和24小时被评估.
主要成果:
- 用车辆治疗的老鼠的受伤动脉在2小时后显示了粘附分子,化学吸引剂 (CINC-2beta,MCP-1) 和细胞因子 (IL-1,IL-6) 的mRNA显著增加 (2-5000倍).
- 2小时后,E2显著减弱了这些介质的表达 (60-80%).
- E2 抑制了中性粒细胞的化学反应活性 65%,并降低了 CINC-2alpha 表达.
结论:
- 雌激素 (E2) 减弱了早期的血管损伤反应.
- 在某种程度上,E2通过负调节促炎媒介体的表达来实现这一目标.
- 这导致受损血管中中性粒细胞的化学反应活性降低.
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