通过深海纤维解析化合物FGFC1保护hCMEC/D3细胞之间的紧接综合体
Xiaozhen Diao1,2, Hui Han1, Haoyu Sun1
1Department of Marine Bio-Pharmacology, College of Food Science and Technology, Shanghai Ocean University, Shanghai 201306, China.
Marine drugs
|August 28, 2024
概括
深海化合物FGFC1通过增强紧密结合蛋白质claudin-5和VE-cadherin来保护血脑屏障的完整性免受氧化应激. 这一发现支持FGFC1的说法.
科学领域:
- 神经科学是一个神经科学.
- 生物化学 生物化学
- 细胞生物学 细胞生物学
背景情况:
- 紧结复合体 (TJCs) 对血脑屏障 (BBB) 的完整性至关重要.
- hCMEC/D3细胞在体外模拟BBB用于研究.
- 氧化应激可以损害BBB功能.
研究的目的:
- 研究FGFC1对H2O2诱导的TJC功能障碍的保护作用.
- 阐明FGFC1作用背后的分子机制.
- 评估FGFC1在血栓消毒治疗中预防出血并发症的潜力.
主要方法:
- 在实验室模型中使用hCMEC/D3细胞.
- 温度校正的超内皮电阻 (tcTEER) 的测量.
- 免疫光显微镜 (IFM) 和定量实时PCR (qRT-PCR) 用于蛋白质和基因表达.
- 分子对接模拟. 分子对接模拟.
主要成果:
- H2O2 (1 mM) 降低了BBB完整性,由降低的tcTEER表示.
- FGFC1 (80-100μM) 显著抑制了H2O2诱导的tcTEER下降.
- FGFC1在转录层面上调节了克劳丁-5 (CLDN-5) 和 VE-cadherin (VE-cad) 的表达.
- 分子对接确认了FGFC1的目标CLDN-5和VE-cad.
结论:
- FGFC1保护BBB完整性免受H2O2引起的损伤.
- FGFC1通过上调CLDN-5和VE-cad来发挥其保护作用.
- FGFC1在治疗脑血栓的血栓消化药物治疗期间减少出血风险方面显示出有前途.
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