氨基和毫林对心肌炎炎症信号的不同影响
Nikhil K Chanani1, Douglas B Cowan, Koh Takeuchi
1Department of Anesthesia, Children's Hospital and Harvard Medical School, Boston, Mass 02115, USA.
Circulation
|October 2, 2002
概括
氨通过抑制核因子-卡帕B (NFkappaB) 激活和促炎性细胞因子产生来减少心脏炎症. 然而,米利诺会加剧心肌细胞中的这些炎症反应.
科学领域:
- 心血管生物学 心血管生物学
- 炎症研究 炎症研究
- 药理学 药理学是指药理学的学科.
背景情况:
- 系统和局部炎症性细胞因子与心肌功能障碍有关,例如缺血再输和心力衰竭.
- 固酶抑制剂 (PDEI) 在这些情况下使用,可能调节炎症信号,但机制尚不清楚.
研究的目的:
- 为了研究氨和米利对心脏细胞炎症反应的影响.
- 阐明这些固酶抑制剂影响炎症信号通路的机制.
主要方法:
- 主要大鼠心肌细胞培养物被用脂多糖 (LPS) 或瘤亡因子-α (TNF-α) 治疗,含有或不含有阿姆里或米利.
- 评估核因子-kappa B (NFkappaB),氧化合成酶 (iNOS),环氧化原酶-2 (COX-2) 和细胞因子生产的调节,使用电泳运动转移测定,西方免疫血栓和ELISA.
- 研究了周期性腺单酸盐 (cAMP) 和周期性关单酸盐 (cGMP) 在调解这些效应中的作用.
主要成果:
- 氨显著降低了LPS/TNF-α诱导的NFkappaB激活,iNOS和细胞因子的产生,但没有减少COX-2的表达.
- 米利诺增加了NFkappaB转位,iNOS和COX-2表达,以及互白素-1β的产生.
- 细胞透性cAMP模仿炎症基因表达,而cGMP没有影响,这表明amrinone的作用不仅仅是由于固酶抑制.
结论:
- 氨通过降低NFkappaB激活和心脏细胞中促炎性细胞因子的产生来表现出抗炎作用.
- 米利诺表现出促炎作用,增加关键的炎症标志物和细胞因子的产生.
- 这些发现突显了PDEI对心脏炎症信号通路的影响.
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