Evidence map›Paper›PMID 35622215›Full record

ArticleNeurochemical research2022

Electroacupuncture Promotes Autophagy by Regulating the AKT/mTOR Signaling Pathway in Temporal Lobe Epilepsy.

Dongsheng Gao, Linqing Ma, Yunliang Xie, Bo Xiao, Shouru Xue, Wenbiao Xiao, You Zhou, Xiuying Cai, Xiaoyan Yang

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Trial
  2. Article
  3. NEAT1 Promotes Epileptogenesis in Tuberous Sclerosis Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  5. Article
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  8. Review
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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

9 authors at 4 institutions in 1 country.

Dongsheng Gao *The People's Hospital of Suzhou New District, Suzhou, China.
Linqing Ma *The People's Hospital of Suzhou New District, Suzhou, China.
Yunliang Xie *The People's Hospital of Suzhou New District, Suzhou, China.
Bo XiaoDepartment of Neurology, Xiangya Hospital, Central South University, Changsha, China.
Shouru XueDepartment of Neurology, The First Affiliated Hospital of Suzhou University, 899 Pinghai Road, Suzhou, Jiangsu, China.
Wenbiao XiaoDepartment of Neurology, Xiangya Hospital, Central South University, Changsha, China.
You ZhouThe People's Hospital of Suzhou New District, Suzhou, China.
Xiuying CaiDepartment of Neurology, The First Affiliated Hospital of Suzhou University, 899 Pinghai Road, Suzhou, Jiangsu, China. cxy9990888@163.com.
Xiaoyan YangThe People's Hospital of Suzhou New District, Suzhou, China. yangxiaoyan2021@foxmail.com.ORCID http://orcid.org/0000-0002-0155-3200
The Fifth People’s Hospital of Suzhou · CNCentral South University · CNCixian People's Hospital · CNSoochow University · CN

Funding

2019 Suzhou Livelihood Science and Technology Guidance Project SYSD2019078Medical and health science and technology project of Suzhou High-tech Zone 2018Z002Scientific Innovation Fund project of Suzhou High-tech Zone People's Hospital SGY2018B01
6 · The paper itself

Abstract

Temporal lobe epilepsy (TLE) is a complex neurological disease, and its occurrence and development are closely related to the autophagy signaling pathway. However, the mechanism by which electroacupuncture (EA) affects the regulation of autophagy has not been fully elucidated. TLE gene chip dataset GSE27166 and data from rats without epilepsy (n = 6) and rats with epilepsy (n = 6) were downloaded from Gene Expression Omnibus. The differentially expressed genes (DEGs) in the TLE and control groups were identified with the online tool GEO2R. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases were used to analyse the functional and pathway enrichment of genes in the most important modules. A rat model of TLE induced by lithium-pilocarpine treatment was established. EA treatment at DU20 and DU14 in TLE rats was performed for 2 weeks. Neuronal regeneration was determined using immunofluorescence staining. The protein levels of AKT/mTOR signaling pathway and autophagy markers were detected through western blotting and immunohistochemistry. This study identified 1837 DEGs, including 798 upregulated genes and 1039 downregulated genes. GO enrichment and KEGG analyses were performed on DEGs and revealed functional enrichment mainly in the mTOR signaling pathway and autophagy-animal. Furthermore, the number of mature neurons was significantly increased upon coexpressing BrdU/NeuN in TLE rats treated with EA. Western blotting and immunohistochemistry results showed significantly decreased levels of the phosphorylated-AKT and p-mTOR in the hippocampal CA3 and DG regions of TLE rats with EA treatment. And increased p-ULK1/ULK1, LC3-II/LC3-I and p62 levels in TLE rats with EA stimulation. Therefore, this study suggested that EA promoted autophagy in hippocampal neurons during the onset of epilepsy by regulating the AKT/mTOR signaling pathway to treat epilepsy.

Indexed as

ElectroacupunctureEpilepsy, Temporal LobeAnimalsAutophagyProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleySignal TransductionTOR Serine-Threonine KinasesmTOR protein, ratProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesElectroacupunctureHippocampusmTOR signaling pathwayNeurologyTemporal lobe epilepsy

Identifiers

PMID35622215
OpenAlexW4281692582

What OpenQuestion holds

Textmetadata
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.