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沃贡因减轻了后的微质介导的突触过度修剪和认知障碍

Yang Hu¹, Honggang Qi¹, Jiurong Yang¹

¹Department of Pharmacology, Jiangsu Provincial Key Laboratory of Critical Care Medicine, Medical School of Southeast University, Nanjing, China.

Phytomedicine : international journal of phytotherapy and phytopharmacology

|November 15, 2024

概括

沃贡尼是一种天然化合物,可以减少中微质细胞过度的突触修剪,改善小鼠的认知功能. 这种神经保护作用是由AKT/FoxO1通路介导的.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
药理学药理学是指药理学的学科.

背景情况:

涉到反复发生的神经元放电,导致大脑功能障碍和严重的患者负担.
中枢神经系统 (CNS) 中激活的微质细胞可以过度削减突触,恶化相关的神经元损伤和认知衰退.
黄胺,一种黄胺,显示神经保护,但其对中的微质激活和突触修剪的影响尚不清楚.

研究的目的:

在的小鼠模型中调查沃贡宁对微质激活,突触修剪和认知功能的影响.
阐明伏戈宁作用背后的分子机制,特别是其对AKT/FoxO1通路的影响.

主要方法:

一种皮洛卡尔诱导的病小鼠模型被用来评估突触密度 (Synaptophysin,PSD-95) 和微细胞.
沃贡尼 (50和100毫克/公斤) 通过腹膜内注射,随后进行行为测试 (Y迷宫,物体识别,莫里斯水迷宫).
使用单细胞测序和途径分析 (AKT/FoxO1) 来了解微质状态的改变.

主要成果:

患有的小鼠表现出活化的微质细胞与增加的细胞分裂和减少的突触标记物 (Synaptophysin,PSD-95).
沃贡尼治疗 (100 mg/kg) 显著恢复了突触密度,改善了记忆力和认知缺陷.
发现wogonin通过AKT/FoxO1通路激活来抑制微质前炎性细胞因子释放和突触细胞分裂.

结论:

沃戈宁有效地缓解了中微细胞过度的突触修剪.
沃贡尼治疗通过AKT/FoxO1通路改善了性小鼠的认知功能障碍.
沃戈宁通过调节神经炎症和突触完整性,显示出作为的治疗剂的潜力.

关键词:

在 AKT AKT 里面.认知功能障碍认知功能障碍是一种病.微质细胞中的微质细胞突触剪裁是指突触剪裁.在Wogonin中工作.

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