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拉巴胺素和苏拉明对TNF-介导性母细胞和大脑微血管内皮细胞功能障碍的影响

Katherine A Ebbert¹, Rui Chen¹, Robert A Culibrk¹

¹Department of Biomedical Engineering, Rensselaer Polytechnic Institute, Troy, New York, USA.

Biotechnology and bioengineering

|October 22, 2025

概括

这项研究探讨了炎症期间大脑内皮细胞和免疫细胞如何相互作用. 苏拉明部分改善了血脑屏障功能,但没有解决免疫细胞激活,这表明复杂的治疗挑战.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
细胞生物学细胞生物学

背景情况:

慢性血脑屏障 (BBB) 的破坏与神经退行性疾病有关.
损伤的大脑微血管内皮细胞 (BMEC) 和免疫细胞相互作用有助于BBB功能障碍.
该Akt/mTOR/GSK通路对于血管生成和免疫细胞激活至关重要,提供潜在的治疗点.

研究的目的:

在炎症条件下 (TNF-α) 调查BMEC和巨细胞 (MC) 功能障碍.
分析Akt/mTOR/GSK通路在BMEC-MC交叉声调中的作用.
为了比较苏拉和拉巴胺对炎症反应和BBB完整性的影响.

主要方法:

使用了初级人类BMEC和HMC-1.2巨细胞系.
用TNF-α刺激细胞,并用苏拉或拉巴胺治疗.
测量包括氧化应激 (PGE2),细胞因子/化学因子的产生,以及途径中间酸化 (p-p70S6K,p-RPS6,p-GSK3α/β).

主要成果:

TNF-α刺激增加了氧化应激,促炎性细胞因子和BMEC和MC中的通路激活.
培养在MC中加剧了细胞内细胞因子水平,拉巴胺对细胞外介质具有适度的影响.
苏拉明降低了细胞外炎症标志物,增加了PDGF-BB (BBB稳定),但也增加了细胞内BMEC细胞因子,并没有解决MC激活.

结论:

TNF-α诱导显著的BMEC和MC功能障碍和炎症交叉声.
苏拉明显示了部分BBB保护作用,但未能完全解决MC介导的炎症.
准Akt/mTOR/GSK通路为神经炎症性BBB干扰提供了复杂的治疗潜力.

关键词:

阿尔茨海默病的疾病阿尔茨海默病的疾病.大脑的微血管内皮细胞.巨细胞巨细胞神经炎症是一种神经炎症.这种药物是拉帕米辛 (Rapamycin).苏拉明·苏拉明 (suramin suramin) 是一种

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