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诺奇1依赖性海马细胞亡与单克罗他林诱导的焦虑类行为有关

Lai Baochang¹, Li Fan², Wang Fei³

¹Department of Peripheral Vascular, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China; Cardiovascular Research Center, Xi'an Jiaotong University, Xi'an 710061, China.

|November 28, 2025

概括

莫诺克罗塔林中毒通过诱导海马神经元亡,导致类似焦虑的行为. 这种神经毒性是由Notch1/caspase-3途径调解的,提供了一个潜在的治疗点.

科学领域:

神经科学是一个神经科学.
毒理学毒理学毒理学
药理学药理学是指药理学的学科.

背景情况:

单克罗他林 (MCT) 诱导肺高血压和神经毒性.
MCT诱导的焦虑障碍的机制尚未完全理解.
海马是一个关键的大脑区域,参与焦虑.

研究的目的:

为了阐明MCT诱导的焦虑类行为的分子机制.
研究Notch1/caspase-3通路在MCT神经毒性中的作用.
评估向这种途径的治疗潜力.

主要方法:

给大鼠服用MCT (60mg/kg) 持续4周,以诱导焦虑和肺高血压.
行为测试 (开放场,高空加迷宫) 评估了类似焦虑的行为.
使用H&E和Annexin V-FITC/PI染色来评估海马细胞亡.
西方斑点分析了亡标记物 (caspase-3) 和Notch1信号.
使用siRNA和DAPT抑制剂抑制了诺奇1.

主要成果:

在老鼠中,MCT的使用增加了类似焦虑的行为.
在活体和体外,MCT诱导了海马神经元的亡.
MCT增加了酶-3的激活和Notch1的表达.
诺奇1抑制 (siRNA或DAPT) 降低了MCT诱导的亡和caspase-3激活.
DAPT治疗缓解了类似焦虑的行为和海马细胞亡.

结论:

MCT通过Notch1/caspase-3通路诱导焦虑类行为和海马神经毒性.
准Notch1/caspase-3通路可能是治疗MCT诱导的神经毒性和焦虑障碍的可行策略.

关键词:

类似焦虑的行为.在Caspase-3中使用.海马体的亡是海马体的亡.单克罗他林 (Monocrotaline) 是一种可怕的药物.标记1 标记1 标记

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Notch Signaling Pathway

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