在阿尔茨海默氏症模型中,利科哈尔科恩A通过抑制内分泌网膜压力介导的亡来改善认知功能障碍
Yun Fan1, Yun Ling1, Xibin Zhou1
1School of Traditional Chinese Medicine, Nanjing University of Traditional Chinese Medicine, Nanjing, China.
Journal of geriatric psychiatry and neurology
|October 22, 2024
概括
利科哈尔科恩A (Lico A) 改善了阿尔茨海默氏症的发生.
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.
- 分子生物学分子生物学
背景情况:
- 阿尔茨海默氏症 (AD) 与由内质网膜 (ER) 压力引起的神经退行有关.
- 来自Glycyrrhiza物种的黄类药物Licochalcone A (Lico A) 正在研究其在AD的潜在治疗作用.
研究的目的:
- 在AD模型中调查Lico A对认知障碍的有益影响.
- 阐明Lico A调节ER压力和神经元亡的机制.
主要方法:
- 三重转基因小鼠AD模型被用LicoA (5或15毫克/公斤) 治疗.
- 评估了认知功能,Aβ沉积,ER压力标志物和神经元亡.
- 主要海马神经元被用来探索涉及特定抑制剂的分子机制.
主要成果:
- 在AD小鼠中,LicoA治疗改善了认知缺陷并减少了Aβ斑块.
- 在体内和体外模型中,Lico A抑制了ER应激和神经元亡.
- 利科A的保护作用部分通过Nrf2和PI3K通路进行介导.
结论:
- 利科A改善ER压力诱导的神经退行以及阿尔茨海默病的认知障碍.
- 利科A通过调节PERK/eIF2α/ATF4/CHOP信号通路来证明AD的治疗潜力.
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