Evidence map›Paper›PMID 40256391›Full record

ArticleFrontiers in aging neuroscience2025

Galangin reduces MPTP-induced dopamine neuron injury via the autophagy dependent-PI3K/AKT pathway.

Liping Huang, Qiaofeng Li, Jingyi Wu, Yingying He, Junwei Huang, Sipeng Xie, Canfeng Yang, Qingling Ruan, Zhongliu Zhou, Minzhen Deng

Abstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
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

10 authors.

Liping HuangSchool of Chemistry and Chemical Engineering, Western Guangdong Characteristic Biomedical Engineering Technology Research Center, Lingnan Normal University, Zhanjiang, China.
Qiaofeng LiSchool of Chemistry and Chemical Engineering, Western Guangdong Characteristic Biomedical Engineering Technology Research Center, Lingnan Normal University, Zhanjiang, China.
Jingyi WuSchool of Chemistry and Chemical Engineering, Western Guangdong Characteristic Biomedical Engineering Technology Research Center, Lingnan Normal University, Zhanjiang, China.
Yingying HeSchool of Chemistry and Chemical Engineering, Western Guangdong Characteristic Biomedical Engineering Technology Research Center, Lingnan Normal University, Zhanjiang, China.
Junwei HuangSchool of Chemistry and Chemical Engineering, Western Guangdong Characteristic Biomedical Engineering Technology Research Center, Lingnan Normal University, Zhanjiang, China.
Sipeng XieSchool of Chemistry and Chemical Engineering, Western Guangdong Characteristic Biomedical Engineering Technology Research Center, Lingnan Normal University, Zhanjiang, China.
Canfeng YangSchool of Chemistry and Chemical Engineering, Western Guangdong Characteristic Biomedical Engineering Technology Research Center, Lingnan Normal University, Zhanjiang, China.
Qingling RuanSchool of Chemistry and Chemical Engineering, Western Guangdong Characteristic Biomedical Engineering Technology Research Center, Lingnan Normal University, Zhanjiang, China.
Zhongliu ZhouSchool of Chemistry and Chemical Engineering, Western Guangdong Characteristic Biomedical Engineering Technology Research Center, Lingnan Normal University, Zhanjiang, China.
Minzhen DengState Key Laboratory of Traditional Chinese Medicine Syndrome/ Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Research has confirmed that Galangin can attenuate autophagy and protect dopaminergic neurons. This study aims to clarify whether Galangin attenuates dopaminergic neuron injury by regulating the PI3K/AKT pathway in Parkinson's disease (PD) model mice. Methods: The study explores the mitigating effects of Galangin on PD processes by administering 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to induce the condition. Techniques including network analysis, transcriptomic analysis, rotarod test, enzyme-linked immunosorbent assay (ELISA), qRT-PCR, western blotting, immunohistochemistry, immunofluorescence, and hematoxylin-eosin (HE) were employed to unveil the molecular changes induced by Galangin. Results: The network pharmacological analysis showed 301 targets related to Galangin, and 2,858 genes related to PD. Galangin treatment can improve the motor coordination of PD model mice, reduce damage to neurons in the brain, improve the antioxidant capacity and reduce the inflammatory damage of brain tissue. Additionally, Galangin suppressed mRNA expression of PD markers (IL-1β, TNF- Conclusion: Galangin supresses Beclin-1-dependent autophagy and upregulates the PI3K/AKT signaling pathway to attenuate the neuroinflammatory injury and improve motor coordination ability in PD mice induced by MPTP.

Indexed as

autophagyGalanginnetwork analysisParkinson’s diseasetranscriptomics

Identifiers

PMID40256391
PMCPMC12006098

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.