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在脊髓损伤后,BHLHE40通过NF-κB通路调节微质偏振

Chao Ma¹, Yansong Wang²

¹Department of Orthopedic Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.

Brain research bulletin

|November 25, 2024

概括

在脊髓损伤 (SCI) 中击倒Bhlhe40可以减少神经炎症和神经元损失. 这种有针对性的方法通过通过NF-κB通路调节微质极化来促进功能恢复.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

脊髓损伤 (SCI) 导致神经炎症和神经元死亡.
Bhlhe40是一种应激反应的转录因子,与炎症有关.
目前尚不清楚Bhlhe40在SCI病原发生中的作用.

研究的目的:

研究Bhlhe40在SCI中的表达和功能.
确定Bhlhe40敲击是否影响神经炎症,神经元损失和SCI后的功能恢复.
阐明Bhlhe40在SCI中的作用背后的分子机制,重点关注微质极化和NF-κB通路.

主要方法:

已建立的SCI老鼠模型使用动脉瘤剪贴.
使用lentiviral Bhlhe40 shRNA在体内抑制Bhlhe40的表达.
在体外实验中,使用用LPS和IFN-γ刺激的BV2微细胞来诱导M1极化.
评估了神经炎症,神经元亡,微质两极分化,促炎细胞因子水平 (TNF-α,IL-1β,IL-6) 和NF-κB通路激活.

主要成果:

在受伤的脊髓组织中,Bhlhe40表达显著上调.
Bhlhe40 Knockdown 降低了神经炎症,减轻了神经元损失,并改善了神经功能恢复.
Bhlhe40缺乏抑制了M1微质的两极分化,并降低了促炎性细胞因子的分泌.
敲除Bhlhe40抑制了SCI大鼠和体外微细胞模型中的NF-κB信号通路.

结论:

在SCI之后,Bhlhe40在恶化神经炎症和神经元损伤方面发挥着至关重要的作用.
Bhlhe40 Knockdown证明了缓解SCI进展的治疗潜力.
Bhlhe40的治疗效果通过抑制M1微质极化和NF-κB通路激活来实现.

关键词:

微质质的两极分化脊髓损伤导致的脊髓损伤在NF-κB路径.基本的螺旋-环-螺旋家族成员e40

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