QKL injection ameliorates Alzheimer's disease-like pathology by regulating expression of RAGE

被引：0
|
作者：
Dou, Jinfang [1 ]
Zhang, Xin 'ai [2 ]
Hu, Chaoqun [1 ]
Gao, Yuqian [3 ]
Zhao, Yue [3 ]
Hei, Murong [3 ]
Wang, Zhimiao [1 ]
Guo, Nan [3 ]
Zhu, Haiyan [1 ,3 ]
机构：
[1] Beijing Univ Chinese Med, Beijing, Peoples R China
[2] China Acad Chinese Med Sci, Guanganmen Hosp, Beijing, Peoples R China
[3] Beijing Univ Chinese Med, Dongzhimen Hosp, Beijing 100700, Peoples R China
来源：
EXPERIMENTAL GERONTOLOGY | 2024年 / 190卷
基金：
中国国家自然科学基金;
关键词：
beta-Amyloid; QKL injection; Receptor for advanced glycation end products; Network pharmacology; Molecular docking; AMYLOID-BETA; SYNAPTIC DAMAGE; STRESS; BRAIN; MODEL;
D O I：
10.1016/j.exger.2024.112422
中图分类号：
R592 [老年病学]; C [社会科学总论];
学科分类号：
03 ; 0303 ; 100203 ;
摘要：
The onset of Alzheimer's disease is related to neuron damage caused by massive deposition of A beta in the brain. Recent studies suggest that excessive A beta in the brain mainly comes from peripheral blood, and BBB is the key to regulate A beta in and out of the brain. In this study, we explored the pathogenesis of AD from the perspective of A beta transport through the BBB and the effect of QKL injection in AD mice. The results showed that QKL could improve the cognitive dysfunction of AD mice, decrease the level of A beta and A beta transporter-RAGE, which was supported by the results of network pharmacology, molecular docking and molecular dynamics simulation. In conclusion, RAGE is a potential target for QKL's therapeutic effect on AD.
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页数：10
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