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QKL injection ameliorates Alzheimer's disease-like pathology by regulating expression of RAGE.
Dou, Jinfang; Zhang, Xin'ai; Hu, Chaoqun; Gao, Yuqian; Zhao, Yue; Hei, Murong; Wang, Zhimiao; Guo, Nan; Zhu, Haiyan.
Affiliation
  • Dou J; Beijing University of Chinese Medicine, Beijing, China.
  • Zhang X; Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
  • Hu C; Beijing University of Chinese Medicine, Beijing, China.
  • Gao Y; Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing, China.
  • Zhao Y; Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing, China.
  • Hei M; Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing, China.
  • Wang Z; Beijing University of Chinese Medicine, Beijing, China.
  • Guo N; Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing, China. Electronic address: brandy396@163.com.
  • Zhu H; Beijing University of Chinese Medicine, Beijing, China; Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing, China. Electronic address: zhuhaiyangy@163.com.
Exp Gerontol ; 190: 112422, 2024 Jun 01.
Article in En | MEDLINE | ID: mdl-38599502
ABSTRACT
The onset of Alzheimer's disease is related to neuron damage caused by massive deposition of Aß in the brain. Recent studies suggest that excessive Aß in the brain mainly comes from peripheral blood, and BBB is the key to regulate Aß in and out of the brain. In this study, we explored the pathogenesis of AD from the perspective of Aß 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 Aß and Aß 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.
Subject(s)
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Amyloid beta-Peptides / Disease Models, Animal / Alzheimer Disease / Receptor for Advanced Glycation End Products Limits: Animals Language: En Journal: Exp Gerontol Year: 2024 Document type: Article

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Amyloid beta-Peptides / Disease Models, Animal / Alzheimer Disease / Receptor for Advanced Glycation End Products Limits: Animals Language: En Journal: Exp Gerontol Year: 2024 Document type: Article