在巨细胞中通过Akt-NFκB通路引起的环素诱导的前炎性反应
Hao-Min Wu1, Chen-Yu Chiang2, Wen-Ying Chen2
1Department of Cardiology, Kaohsiung Armed Forces General Hospital, Kaohsiung City, Taiwan.
Environmental toxicology
|August 8, 2023
概括
环素是一种抗胰岛素,可以过度激活巨细胞,增加TNF-α和IL-6等炎症性细胞因子. 这通过Akt-NFκB通路发生,可能导致不良影响.
科学领域:
- 免疫学 免疫学 免疫学
- 药理学 药理学是指药理学的学科.
背景情况:
- 环氨酸用于恶心,吐和运动性恶心,具有抗胺和抗肌肉性质.
- 巨细胞的激活对于天生的免疫力至关重要,但过度激活会导致有害的炎症反应.
- 滥用cyclizine与严重的神经和心理影响有关,包括混乱,和自杀念头.
研究的目的:
- 调查环素对巨细胞激活和潜在的分子机制的影响.
- 为了确定环素是否影响巨细胞中促炎媒介体的产生.
主要方法:
- 巨细胞被用环素治疗.
- 测量了促炎性细胞因子 (TNF-α,IL-1β,IL-6) 和氧化 (NO) 的水平.
- 评估了Akt-NFκB信号通路的激活,包括Akt和NFκB p65的酸化.
主要成果:
- 环素显著增强了促炎性细胞因子的产生:瘤缩因子-α (TNF-α),介质素-1β (IL-1β) 和介质素-6 (IL-6).
- 通过对可诱导的氧化合成酶 (iNOS) 表达的上调调节,cyclizine诱导氧化 (NO) 分泌.
- 循环治疗导致Akt和核因子-kappa B (NFκB) p65的酸化增加,表明Akt-NFκB通路的激活.
结论:
- 环素激活巨细胞,促进促炎性细胞因子和媒介的释放.
- 该Akt-NFκB信号通路参与调解巨细胞中循环诱导的炎症反应.
- 这些发现表明,可能存在一种机制,将cyclizine的药理作用与炎症过程联系起来.
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