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奎尔塞塔吉特林改善与APP/PS1小鼠TNFα/NFκB通路相关的类似阿尔茨海默氏症的病态

Cuiyi Yuan¹, Shuting Lv¹, Yuping Han¹

¹Brain Disease and Big Data Research Institute, College of Life Sciences and Oceanography, Shenzhen University, Shenzhen 518060, China.

|November 3, 2025

概括

在阿尔茨海默氏病 (AD) 模型中,奎尔塞塔吉特林有效降低神经炎症和粉样β病理. 这种天然化合物向TNFα,为AD治疗提供了一个有前途的治疗途径.

科学领域:

神经科学是一个神经科学.
药理学药理学是一个学科.
生物化学生物化学

背景情况:

阿尔茨海默病 (AD) 的特点是粉样β (Aβ) 斑块和团.
神经炎症由TNFα和NFκB调节,是AD病变发生的组成部分.
开发针对阿尔茨海默病的新型治疗药物是一个至关重要的未得到满足的需求.

研究的目的:

调查quercetagitrin在阿尔茨海默病中的治疗潜力和潜在机制.
利用网络药理学和体内模型来探索Quercetagitrin对AD病理学的影响.

主要方法:

网络药理学预测奎塞塔吉特林的主要标是TNFα.
分子对接证实了奎塞塔基特林和TNFα之间的高亲和结合.
在APP/PS1小鼠的体内研究评估了行为,生化和组织学结果.

主要成果:

在AD小鼠中,Quercetagitrin显著降低了TNFα水平,并抑制了NFκB信号传递.
用西西特林治疗改善了Aβ病理和认知缺陷.
在AD小鼠模型中,Quercetagitrin表现出抗神经炎症作用.

结论:

奎尔塞塔吉特林在阿尔茨海默病中表现出治疗潜力.
该化合物的机制涉及向TNFα和调节神经炎症.
这些发现支持quercetagitrin作为AD药物开发的候选药物.

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