埃达拉脱醇通过抑制TLR4/MyD88/NF-κB通路,促进M2微质两极分化,对抗脂多糖诱导的炎症

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Depletion and Reconstitution of Macrophages in Mice
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Depletion and Reconstitution of Macrophages in Mice

Published on: August 1, 2012

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Jing Huang1, Xiaohui Hu1, Juanqin Li1

  • 1Department of Neurology, Jingzhou Hospital Affiliated to Yangtze University, Jingzhou, China.

Naunyn-Schmiedeberg's archives of pharmacology
|March 15, 2024
PubMed
概括

埃达拉 (ED) 将微质从炎症M1状态转移到抗炎M2状态. 这种新型化合物通过抑制TLR4/NF-κB通路来减少神经炎症,并提供抗氧化功效.

关键词:
在BV-2微质上埃达拉 (EDARAVONE) 是一种使用德克斯波诺醇 (DEXBORNOL) 的药物.脂聚糖类糖化物 脂聚糖类糖化物两极化的偏化通过TLR4/MyD88/NF-κB通路进行.

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