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针对MAD2B作为缺血性中风治疗的策略

Lijing Zhang¹, Hengzhen Cui¹, Wandi Hu¹

¹Department of Neurobiology, School of Basic Medical Sciences, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

Journal of advanced research

|July 7, 2024

概括

通过通过ROCK2.2.减少神经元亡,MAD2B抑制改善了中风后的认知功能. 这一发现为中风后认知障碍提供了潜在的治疗标.

科学领域:

神经科学是一个神经科学.
细胞生物学细胞生物学
缺血性中风研究

背景情况:

脑卒中后的认知障碍是脑缺血后残疾的一个重要原因.
作为Cdh1/APC的抑制剂,MAD2B通过神经元中的ROCK2影响突触可塑性和记忆力.
在大脑缺血症中,MAD2B通过ROCK2调节学习和记忆的具体作用尚不清楚.

研究的目的:

研究MAD2B在脑缺血引起的认知功能障碍中的作用.
阐明涉及ROCK2.2的潜在分子机制.

主要方法:

使用了中脑动脉阻塞 (MCAO) 和氧气-葡萄糖剥夺/再氧化 (OGD/R) 模型.
通过透视病毒载体在海马体中生成MAD2B条件淘汰赛小鼠和操纵MAD2B表达.
通过Y-maze和Novel对象识别测试评估认知功能.
分析了MAD2B,ROCK2和与亡相关的分子的表达.
使用抑制剂和shRNA与ROCK2进行干预.

主要成果:

MAD2B的表达在缺血后增加,但在使用神经保护剂时降低.
海马体MAD2B删除改善了MCAO小鼠的认知缺陷和运动协调.
MAD2B删除降低了ROCK2 / LIMK1 / cofilin的调节,并减少了因缺血引起的亡 (BAX,分裂的caspase-3).
在培养的神经元中,ROCK2抑制或淘汰模仿了这些效应.

结论:

通过ROCK2通路促进神经元亡,MAD2B会加剧中风后的认知障碍.
向MAD2B或ROCK2可能是脑缺血引起的神经功能障碍的治疗策略.

关键词:

大脑缺血症的大脑缺血症学习和记忆的学习和记忆这就是MAD2B的意义.神经元神经元是一个神经元.

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