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通过cAMP/PKA/CREB介导的突触和炎症调节来改善与糖尿病相关的认知功能障碍中的Naofucong多目标机制

Mei Ma¹, Yue Tian¹, Ruiying Yin¹

¹Department of Traditional Chinese Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.

CNS neuroscience & therapeutics

|December 23, 2025

概括

在糖尿病相关认知功能障碍 (DACD) 中,Naofucong (NFC) 通过激活cAMP/PKA/CREB通路来改善认知功能. 这种治疗促进突触修复并减少神经炎症,为DACD提供了一个有前途的治疗策略.

科学领域:

神经科学是一个神经科学.
药理学药理学是指药理学的学科.
代谢学代谢学代谢学

背景情况:

糖尿病相关认知功能障碍 (DACD) 是有限治疗的重大并发症.
传统中医药化合物Naofucong (NFC) 显示出神经保护的潜力,但其机制尚不清楚.

研究的目的:

研究NFC对DACD的治疗疗效.
使用多组学和实验验证,阐明NFC影响的分子机制.

主要方法:

采用了一种小鼠模型,在12周内使用NFC治疗的链毒素诱导的DACD.
使用莫里斯水迷宫评估认知表现.
集成的转录和代谢学,通过免疫光学,戈尔吉染色,细胞因子分析,qPCR和西部涂抹进行验证.

主要成果:

NFC显著改善了空间学习和记忆,减少了神经元损伤,并减少了病态蛋白质积累 (APP,p-Tau).
NFC激活了cAMP/PKA/CREB通路,促进了突触修复和调节神经炎症.
通过调节质激活和细胞因子配置,NFC恢复了突触超结构,增强了树突复杂性,调节了神经营养因子和突触蛋白,并通过调节质激活和细胞因子配置重新建立了神经免疫平衡.

结论:

在DACD中,NFC证明了多目标神经保护作用.
NFC的有效性与cAMP/PKA/CREB通路激活,突触可塑性调节和神经炎症调节有关.
NFC是治疗DACD的一个有前途的治疗候选者.

关键词:

在DACDD中,我们可以使用DACDD.没有NFC,没有NFC.cAMP/PKA/CREBEB,这是一个很好的方法.这是一个多主题的多omics.神经炎症是一种神经炎症.突触性可塑性突触性可塑性

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