抑制Notch1信号通过调节中风后的质活动来促进大脑的恢复
Xiaozhu Hao1, Luyi Lin2, Chengfeng Sun1
1Department of Radiology, Huashan Hospital, Fudan University, Shanghai 200040, China.
概括
N-[N-(3,5-difluorophenacetyl)-1-alanyl]-S-phenylglycine t-butylester] (DAPT) 治疗通过转移微质细胞并增强状体的废物排水,但不是皮质,促进大脑恢复. 这表明DAPT是DAPT.
科学领域:
- 神经科学是一个神经科学.
- 神经炎症是一种神经炎症.
- 脑中风恢复 脑中风恢复
背景情况:
- 通过DAPT抑制Notch1信号传递可能会增强中风后的大脑恢复.
- DAPT对条纹体 (STR) 和皮质 (CTX) 恢复的不同影响表明质活动有所不同.
- DAPT对质细胞和恢复的影响的确切机制尚不清楚.
研究的目的:
- 为了调查DAPT是否调节微质亚型转移.
- 为了确定DAPT是否影响星末脚水素-4 (AQP4) 介导的废物溶液排水.
主要方法:
- 在Sprague-Dawley大鼠中,中脑动脉封闭 (MCAO) 模型.
- 治疗组:DAPT (n=5) 和对照组 (n=5).
- 通过24小时和4周的MRI评估,以及中风后4周的免疫光学 (IF).
主要成果:
- 在接受DAPT治疗的老鼠中,MRI显示出 ipsilateral 条纹体的结构恢复,但不是皮质.
- 在两条纹和皮层病变中,IF显示了从促炎M1微质转向抗炎M2微质的转变.
- DAPT治疗在条状周围损伤中增加了AQP4极性,这表明废物排水得到了增强,但在皮质周围损伤中没有.
结论:
- DAPT促进了向保护性微质子类型的转变.
- DAPT增强了状星细胞介导的废物溶液排水.
- 增强的条状体废物溶液代谢可能解释了在条状体和皮质之间观察到的差异性恢复.
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