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

• Published in: Experimental gerontology Vol. 190; p. 112422
• Main Authors: Dou, Jinfang, Zhang, Xin'ai, Hu, Chaoqun, Gao, Yuqian, Zhao, Yue, Hei, Murong, Wang, Zhimiao, Guo, Nan, Zhu, Haiyan
• Format: Journal Article
• Language: English
• Published: England Elsevier Inc 01.06.2024; Elsevier
• Subjects: Alzheimer Disease - drug therapy; Alzheimer Disease - metabolism; Alzheimer's disease; Amyloid beta-Peptides - metabolism; Animals; Blood-Brain Barrier - drug effects; Blood-Brain Barrier - metabolism; Brain - drug effects; Brain - metabolism; Brain - pathology; Cognitive Dysfunction - drug therapy; Cognitive Dysfunction - metabolism; Disease Models, Animal; Male; Mice; Mice, Transgenic; Molecular docking; Molecular Docking Simulation; Molecular Dynamics Simulation; Network pharmacology; QKL injection; Receptor for advanced glycation end products; Receptor for Advanced Glycation End Products - metabolism; β-Amyloid; β-Amyloid; Network pharmacology; Receptor for advanced glycation end products; QKL injection; Alzheimer's disease; Molecular docking
• ISSN: 0531-5565; 1873-6815
• DOI: 10.1016/j.exger.2024.112422

The onset of Alzheimer's disease is related to neuron damage caused by massive deposition of Aβ in the brain. Recent studies suggest that excessive Aβ in the brain mainly comes from peripheral blood, and BBB is the key to regulate Aβ in and out of the brain. In this study, we explored the pathogenesis of AD from the perspective of Aβ 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 Aβ and Aβ 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. •QKL injection decreased the Aβ level, and finally improved cognitive impairment in AD mice.•QKL injection inhibited the transport of Aβ by inhibiting the expression of RAGE.•RAGE may be the therapeutic target of QKL, which is proved by the network pharmacology, molecular docking and MDS.