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4,4'-dimethoxychalcone通过激活Keap1/Nrf2信号通路,对阿尔茨海默病小鼠产生神经保护作用

Shanshan Ma¹, Qianqian Wang², Wenzhi Yang³

¹School of Life Sciences, Zhengzhou University, Zhengzhou 450001, Henan, China; International Joint Research Laboratory for Regenerative Medicine and Neurofunctional Repair of Henan Province, Zhengzhou 450001, Henan, China.

European journal of pharmacology

|January 31, 2026

概括

4,4'-Dimethoxychalcone (DMC) 在阿尔茨海默氏症 (AD) 治疗方面显示出有前途. 通过激活Keap1/Nrf2通路,DMC治疗改善了小鼠的认知功能,并减少了AD病理.

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.
生物化学生物化学

背景情况:

阿尔茨海默病 (AD) 是一种进展性神经退行性疾病,缺乏有效的治疗方法.
4,4'-Dimethoxychalcone (DMC),一种天然的石墨烯,已知可以促进自并延长寿命.
在AD中DMC的神经保护潜力和潜在机制在很大程度上仍未被探索.

研究的目的:

在阿尔茨海默病的小鼠模型中研究DMC的神经保护作用.
阐明DMC发挥其作用的分子机制,重点关注Keap1/Nrf2信号通路.

主要方法:

用DMC治疗5×FAD转基因小鼠.
评估认知功能,抑郁行为,血脑屏障完整性,粉样蛋白-β病理和p-Tau表达.
在体内和体外评估质细胞激活,神经发生和氧化应激标志物.
使用Brusatol,一个Keap1/Nrf2信号抑制剂,以确认途径的参与.

主要成果:

在5×FAD小鼠中,DMC治疗显著改善了认知和抑郁行为.
DMC改善了血脑屏障的透性,减少了粉样β病理,并抑制了p-Tau的表达.
通过激活Keap1/Nrf2通路,DMC抑制了质激活,增强了神经发生,并降低了氧化应激.
抑制Keap1/Nrf2信号传递部分逆转了DMC的神经保护作用.

结论:

在阿尔茨海默氏病的小鼠模型中,DMC显示出显著的神经保护作用.
DMC的神经保护机制涉及到Keap1/Nrf2信号通路的激活.
DMC代表了阿尔茨海默氏症的潜在治疗候选者,需要进一步调查.

关键词:

4,4'-Dimethoxychalcone 是一种有氧化.阿尔茨海默氏症的疾病是阿尔茨海默氏症.凯普1/Nrf2信号传输神经保护是一种神经保护.氧化应激是一种氧化应激.

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