Evidence map›Paper›PMID 39563386›Full record

ArticleAlzheimer's research & therapy2024

Unveiling the molecular mechanisms of Danggui-Shaoyao-San against Alzheimer's disease in APP/PS1 mice via integrating proteomic and metabolomic approaches.

Qihui Wu, Wei Wang, Zhuangzi Huang, Xianghao Lin, Maozhong Yao, Chuipu Cai, Guohu Weng, Yong Gu, Hongying Li, Jinman Liu and 2 more

Abstract read
In one paragraph

Article in Alzheimer's research & therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Qihui Wu *Clinical Research Center, Hainan Hospital, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, Haikou, 570100, China. wuqh@hainmc.edu.cn.
Wei Wang *Science and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, 510000, China.
Zhuangzi HuangClinical Research Center, Hainan Hospital, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, Haikou, 570100, China.
Xianghao LinSchool of Clinical Medicine, Hubei University of Science and Technology, Xianning, 437100, China.
Maozhong YaoClinical Research Center, Hainan Hospital, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, Haikou, 570100, China.
Chuipu CaiDepartment of Computer Science, Key Laboratory of Intelligent Manufacturing Technology of Ministry of Education, Shantou University, Shantou, 515000, China.
Guohu WengHainan Clinical Center for Encephalopathy of Chinese Medicine, Haikou, 571000, China.
Yong GuClinical Research Center, Hainan Hospital, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou University of Chinese Medicine, Haikou, 570100, China.
Hongying LiCollege of Traditional Chinese Medicine, Hainan Academy of Medical Sciences, Hainan Medical University, Haikou, 571000, China.
Jinman LiuAffiliated Jiangmen TCM Hospital of Ji'nan University, Jiangmen, 529099, China.
Jiansong FangScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, 510000, China. fangjs@gzucm.edu.cn.
Weirong LiScience and Technology Innovation Center, Guangzhou University of Chinese Medicine, Guangzhou, 510000, China. liwr@gzucm.edu.cn.

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2023A1515012148Guangdong Basic and Applied Basic Research Foundation 2023A1515011835Hainan Province Clinical Medical Center [2021] No. 276Hainan Provincial Natural Science Foundation of China 821RC1129Hainan Provincial Natural Science Foundation of China 822MS069National Natural Science Foundation of China 82074505, 82374547National Natural Science Foundation of China 82160956, 82460992Science and Technology Research Project of the Department of Education of Hubei Province No. B2023170TCM Geriatrics Construction Project, Key Discipline of National Administration of TCM 2023No3
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is the most prevalent neurodegenerative disorder for which no effective therapy is currently available. Given that various attempts to target beta-amyloid (Aβ) have been unsuccessful in clinical trials, other potential pathogenic factors such as brain energy metabolism (EM) have attracted increasing attention. Traditional Chinese medicines, including danggui-shaoyao-san (DSS), play a notable role in AD. However, it remains unclear whether DSS exerts therapeutic effects on AD through EM regulation.

methodsIn this study, we conducted behavioural tests, Nissl staining, haematoxylin and eosin staining, and thioflavin S staining, in APP/PS1 mice to assess the pharmacodynamic effect of DSS on AD. Subsequently, we integrated the drug target network of herbal ingredients in DSS and evaluated their absorption, distribution, metabolism, excretion, and toxicity properties to identify the core ingredients. We used proteomic and metabolomic approaches to explore the potential mechanisms of action of DSS against AD. Consequently, we verified the mechanism underlying EM using qPCR, western blotting, and ELISA.

resultsIn vivo experimental results revealed that DSS ameliorated cognitive impairment in APP/PS1 mice, attenuated neuronal apoptosis, and reduced Aβ burden. Furthermore, the drug-target network comprised 6,514 drug-target interactions involving 1,118 herbal ingredients and 218 AD genes, of which 253 were identified as the core ingredients in DSS. The proteomic results implied that DSS could act on EM to alleviate AD, and targeted energy metabolomics suggested that DSS regulated 47 metabolites associated with EM. Mechanistically, we found that DSS could regulate the GSK3β/PGC1α signalling pathway to improve brain glucose uptake and mitigate mitochondrial dysfunction and oxidative stress, ultimately promoting EM to treat AD.

conclusionOur study is the first to integrate multi-omics approaches to reveal that DSS could regulate the GSK3β/PGC1α signalling pathway to exert therapeutic effects in AD through the promotion of EM, thereby providing new insights into the mechanism of action of DSS against AD.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorDrugs, Chinese HerbalMice, TransgenicProteomicsAnimalsBrainDisease Models, AnimalMaleMetabolomicsMicePresenilin-1Amyloid beta-Protein Precursordanggui-shaoyao-sanDrugs, Chinese HerbalPresenilin-1Alzheimer’s diseaseDanggui-Shaoyao-SanEnergy metabolismMulti-omics

Identifiers

PMID39563386
PMCPMC11577849

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.