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Mengjiao Zhu^1,2, Si Long³, Yizhi Tao²

¹Department of Anesthesiology, The Central Hospital of Wuhan, Tongji Medical College of Huazhong University of Science and Technology, Nanjing Road, Wuhan, 430030, Hubei Province, China.

Experimental brain research

|November 16, 2023

概括

抑制P38MAPK/ATF2通路可以减少老年小鼠的神经炎症和神经元死亡,改善手术后的认知功能. 这突出了手术期间神经认知障碍 (PND) 的潜在治疗目标.

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.
认知障碍认知障碍认知障碍

背景情况:

海马体中微质介导的神经炎症与外科外神经认知障碍 (PND) 有关.
压力激活P38MAPK信号通路,并在炎症过程中发挥作用.

研究的目的:

研究P38MAPK/ATF2信号通路在老年小鼠中PND发展中的作用.
评估抑制PND这一途径的治疗潜力.

主要方法:

通过骨骨折手术和异氨酸麻醉,建立了PND的老鼠模型.
认知功能使用开放场测试,莫里斯水迷宫 (MWM) 和恐惧条件测试 (FCT) 进行评估.
分析海马组织的炎症因素,亡分子,微质激活 (Iba-1),以及治疗后的神经元存活与P38MAPK抑制剂 (SB239063).

主要成果:

PND小鼠表现出认知障碍,海马前炎症因子 (IL-1β,TNF-α) 的增加,前性分子 (caspase-3,bax) 和微质激活.
SB239063治疗显著降低了这些标记物,并在海马中增加了神经元的存活率.
抑制P38MAPK/ATF2通路减弱了神经炎症和神经元亡.

结论:

P38MAPK/ATF2信号通路与海马神经炎症和神经元亡有关,在老年小鼠中导致PND.
抑制这种途径可以改善PND模型中的认知功能.
准P38MAPK/ATF2通路为预防或治疗PND提供了一个潜在的治疗策略.

关键词:

微质激活的作用神经炎症是一种神经炎症.神经元的亡是神经元的亡.P38MAPK/ATF2信号通道的使用在外科手术期间出现的神经认知障碍.

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