Carotid 动脉血管狭窄导致血液-CSF 屏障受损和神经炎症
Lin Lin1,2,3, Yang Chen2,3, Kai He2,3
1Department of Neurology, The Second Hospital of Dalian Medical University, Dalian, 116027, Liaoning, China.
Journal of neuroinflammation
|September 10, 2024
概括
慢性脑性低流损害了胆管中的血液-脑液屏障,导致神经炎症. 用ZT1a针对SPAK-NKCC1复合体可以减少免疫细胞透并改善认知功能.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 血管生物学 血管生物学
背景情况:
- 冠状腺 (ChP) 通过形成血脑脊髓液 (CSF) 屏障来维持大脑平衡.
- 这种屏障限制了免疫细胞进入中枢神经系统,防止神经炎症.
- 慢性大脑低 perfusion 对CHP结构和屏障完整性的影响尚不清楚.
研究的目的:
- 为了研究慢性大脑低 perfusion 对状交叉体血-CSF 屏障的影响.
- 在这个模型中识别阻碍障碍功能障碍和神经炎症背后的分子机制.
- 评估针对神经炎症中特定途径的治疗潜力.
主要方法:
- 在小鼠中使用双边常见动脉狭窄 (BCAS) 模型来诱导慢性大脑低输液.
- 评估了血液-中枢神经液屏障紧结蛋白,SPAK-NKCC1复合体和免疫细胞透的变化.
- 评估了SPAK抑制 (ZT1a) 对神经炎症和认知功能的疗效.
主要成果:
- BCAS诱导了紧结蛋白 (克劳丁1,克劳丁5) 的改变,并激活了ChP上皮细胞中的SPAK-NKCC1复合体和NF-κB.
- 这种干扰导致巨细胞,微质细胞,中性粒细胞和T细胞透到ChP中.
- 用ZT1a对SPAK的药理阻断减少了BCAS小鼠的免疫细胞透和改善了认知功能.
结论:
- 慢性大脑低流会对胆脉的血液-中枢神经液屏障造成结构性损伤,并促进免疫细胞的透.
- SPAK-NKCC1复合体与大脑低 perfusion 后的神经炎症的发病有关.
- 向SPAK-NKCC1复合体代表了与血管对认知障碍和痴呆的贡献相关的神经炎症的潜在治疗策略.
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