Evidence map›Paper›PMID 41189656›Full record

ArticleFrontiers in neurology2025

Low-frequency electroacupuncture attenuates methamphetamine-induced depressive-like behaviors and cognitive impairment via modulating neuroinflammation.

Jingyi Zhang, Rongji Hui, Jiabao Xu, Ludi Zhang, Bing Xie, Chunling Ma, Yi Li, Yueli Zou, Di Wen, Xiujun Yu

Abstract read
In one paragraph

Article in Frontiers in neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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.

Jingyi Zhang *Key Laboratory of Clinical Neurology, Ministry of Education, Hebei Medical University, Department of Neurology, the Second Hospital of Hebei Medical University, Key Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, China.
Rongji Hui *Hebei Key Laboratory of Forensic Medicine, Collaborative Innovation Center of Forensic Medical Molecular Identification, Research Unit of Digestive Tract Microecosystem Pharmacology and Toxicology, Chinese Academy of Medical Sciences, College of Forensic Medicine, Hebei Medical University, Shijiazhuang, Hebei, China.
Jiabao XuHebei Key Laboratory of Forensic Medicine, Collaborative Innovation Center of Forensic Medical Molecular Identification, Research Unit of Digestive Tract Microecosystem Pharmacology and Toxicology, Chinese Academy of Medical Sciences, College of Forensic Medicine, Hebei Medical University, Shijiazhuang, Hebei, China.
Ludi ZhangHebei Key Laboratory of Forensic Medicine, Collaborative Innovation Center of Forensic Medical Molecular Identification, Research Unit of Digestive Tract Microecosystem Pharmacology and Toxicology, Chinese Academy of Medical Sciences, College of Forensic Medicine, Hebei Medical University, Shijiazhuang, Hebei, China.
Bing XieHebei Key Laboratory of Forensic Medicine, Collaborative Innovation Center of Forensic Medical Molecular Identification, Research Unit of Digestive Tract Microecosystem Pharmacology and Toxicology, Chinese Academy of Medical Sciences, College of Forensic Medicine, Hebei Medical University, Shijiazhuang, Hebei, China.
Chunling MaHebei Key Laboratory of Forensic Medicine, Collaborative Innovation Center of Forensic Medical Molecular Identification, Research Unit of Digestive Tract Microecosystem Pharmacology and Toxicology, Chinese Academy of Medical Sciences, College of Forensic Medicine, Hebei Medical University, Shijiazhuang, Hebei, China.
Yi LiKey Laboratory of Clinical Neurology, Ministry of Education, Hebei Medical University, Department of Neurology, the Second Hospital of Hebei Medical University, Key Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, China.
Yueli ZouKey Laboratory of Clinical Neurology, Ministry of Education, Hebei Medical University, Department of Neurology, the Second Hospital of Hebei Medical University, Key Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, China.
Di WenHebei Key Laboratory of Forensic Medicine, Collaborative Innovation Center of Forensic Medical Molecular Identification, Research Unit of Digestive Tract Microecosystem Pharmacology and Toxicology, Chinese Academy of Medical Sciences, College of Forensic Medicine, Hebei Medical University, Shijiazhuang, Hebei, China.
Xiujun YuKey Laboratory of Clinical Neurology, Ministry of Education, Hebei Medical University, Department of Neurology, the Second Hospital of Hebei Medical University, Key Neurological Laboratory of Hebei Province, Shijiazhuang, Hebei, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Methamphetamine (METH) abuse primarily affects the central nervous system (CNS), leading to CNS damage and contributing to depressive-like behaviors, cognitive impairment, and other neuropsychiatric disorders. Electroacupuncture (EA) has shown promise in treating mental disorders linked to CNS damage, yet the effects of EA on METH-induced depressive-like behaviors and cognitive impairment and it's underlying therapeutic mechanisms remain largely unclear. Methods: In this study, a mouse model of METH-induced neuropsychiatric dysfunction was established by administering high-dose METH under elevated ambient temperature. EA was applied at different frequencies to the Zusanli (ST36) acupoint for 7 days post-METH administration. Results: Behavioral tests revealed that low-frequency EA significantly alleviated depressive-like behaviors and cognitive impairment. Additionally, EA restored blood-brain barrier (BBB) integrity, as evidenced by Western blotting (WB) and Evans blue staining. Neuronal injury was attenuated, as shown by Nissl and hematoxylin and eosin (HE) staining. Further investigations into neuroinflammation revealed that EA suppressed microglial activation in the hippocampus, decreased the expression of IL-6 and TNF- Discussion: The present study suggested that EA alleviates METH-induced depressive-like behaviors and cognitive impairment by modulating neuroinflammation, particularly through the inhibition of microglial activation and pro-inflammatory cytokine release. EA may represent a promising non-pharmacological strategy for the treatment of METH-associated neuropsychiatric disorders.

Indexed as

cognitive impairmentdepressive-like behaviorselectroacupuncturemethamphetamineneuroinflammation

Identifiers

PMID41189656
PMCPMC12580150

What Socratic holds

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LicenceCC BY
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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.