Evidence map›Paper›PMID 29163038›Full record

ArticleFrontiers in molecular neuroscience2017

Electroacupuncture Suppresses the NF-κB Signaling Pathway by Upregulating Cylindromatosis to Alleviate Inflammatory Injury in Cerebral Ischemia/Reperfusion Rats.

Jin Jiang, Yong Luo, Wenyi Qin, Hongmei Ma, Qiongli Li, Jian Zhan, Ying Zhang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Role of CYLD in brain physiology and pathology.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Glial Cells Response in Stroke.Cellular and molecular neurobiology · 2023
    Review
  18. Article
  19. Protective Effects ofMarine drugs · 2021
    Article
  20. 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

7 authors at 3 institutions in 1 country.

Jin JiangDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yong LuoDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Wenyi QinDepartment of Integrated Chinese and Western Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Hongmei MaDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Qiongli LiDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jian ZhanDepartment of Neurology, The Affiliated Hospital of Zunyi Medical College, Zunyi, China.
Ying ZhangDepartment of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Chongqing Medical University · CNFirst Affiliated Hospital of Chongqing Medical University · CNAffiliated Hospital of Zunyi Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Electroacupuncture (EA) may reduce inflammatory injury by inhibiting nuclear factor-kappa B (NF-κB) signaling pathway activation after ischemic stroke. Thus, we explored temporal and spatial expression of cylindromatosis (CYLD), a negative feedback inhibitor of the NF-κB signaling pathway, to learn whether CYLD is essential for EA and reduction of inflammatory injury after focal cerebral ischemia/reperfusion. A middle cerebral artery occlusion/reperfusion (MCAO/R) model was established in male Sprague-Dawley (SD) rats and CYLD gene interference was used to investigate a potential role of neuroprotection. Rats were treated with EA (1 mA, 20 Hz for 5 min, 2 Hz for 30 min) at Baihui (GV 20), Hegu (LI 4) and Taichong (LR 3) acupoints, once daily, beginning 2 h after focal cerebral ischemia. Microglial activation and co-expression of CYLD and NF-κB were measured with immunofluorescence. Neuronal CX3CL1 expression was assayed to investigate the role of EA in the interaction between neurons and microglia via upregulation of CYLD. Then, CYLD, NF-κB p65 and p-IκBα protein expression was measured with Western blot. CYLD was mainly expressed in neurons of the peri-ischemic area after MCAO/R in rats and EA upregulated CYLD mRNA and protein from 24 to 72 h after focal cerebral ischemia/reperfusion. In addition, CYLD overexpression was positively correlated to neurobehavior and negatively connected with infarct volume and pro-inflammatory cytokines (TNF-α and IL-1β). Upregulation of CYLD by EA prevented NF-κB nuclear translocation and inhibition of neuronal CX3CL1 expression, which repressed activation of microglia. Finally, CYLD silencing significantly weakened suppression of the NF-κB signaling pathway by EA. In conclusion, upregulation of CYLD may underlie how EA could alleviate inflammatory injury after focal cerebral ischemia/reperfusion.

Indexed as

cerebral ischemiaCYLDelectroacupuncturemicrogliaNF-κB signaling pathway

Identifiers

PMID29163038
PMCPMC5681846
OpenAlexW2767527972

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Registered trials

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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.