Evidence map›Paper›PMID 34118070›Full record

ArticleClinical and experimental immunology2021

Nuclear factor kappa B inhibitor suppresses experimental autoimmune neuritis in mice via declining macrophages polarization to M1 type.

Donghui Shen, Fengna Chu, Yue Lang, Chao Zheng, Chunrong Li, Kangding Liu, Jie Zhu

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2021. 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
0.8field-weighted citation impact, top 30% 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, 14 citations in OpenAlex.

  1. Salidroside ameliorates experimental autoimmune neuritis by dually modulating neuroinflammation and immune homeostasis via PI3K/AKT signaling.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. 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 2 countries.

Donghui ShenNeuroscience Center, Department of Neurology, The First Hospital of Jilin University, Changchun, China.
Fengna ChuNeuroscience Center, Department of Neurology, The First Hospital of Jilin University, Changchun, China.ORCID 0000-0003-3291-1768
Yue LangNeuroscience Center, Department of Neurology, The First Hospital of Jilin University, Changchun, China.
Chao ZhengNeuroscience Center, Department of Neurology, The First Hospital of Jilin University, Changchun, China.
Chunrong LiNeuroscience Center, Department of Neurology, The First Hospital of Jilin University, Changchun, China.
Kangding LiuNeuroscience Center, Department of Neurology, The First Hospital of Jilin University, Changchun, China.
Jie ZhuNeuroscience Center, Department of Neurology, The First Hospital of Jilin University, Changchun, China.
Jilin University · CNKarolinska University Hospital · SEQingdao University · CN

Funding

National Natural Science Foundation of China 81471216National Natural Science Foundation of China 81671177National Natural Science Foundation of China 81671186Swedish Research Council 2015-03005
6 · The paper itself

Abstract

Guillain-Barré syndrome (GBS) is an acute inflammatory and immune-mediated demyelinating disease of the peripheral nervous system (PNS). Macrophages play a central role in its animal model, experimental autoimmune neuritis (EAN), which has been well accepted. Additionally, nuclear factor (NF)-κB inhibitors have been used to treat cancers and have shown beneficial effects. Here, we investigated the therapeutic effect of M2 macrophage and the NF-κB pathway's correlation with macrophage activation in EAN in C57BL/6 mice. We demonstrate that M2 macrophage transfusion could alleviate the clinical symptoms of EAN by reducing the proportion of M1 macrophage in the peak period, inhibiting the phosphorylation of NF-κB p65. The NF-κB inhibitor (BAY-11-7082) could alleviate the clinical symptoms of EAN and shorten the duration of symptoms by reducing the proportion of M1 macrophages and the expression of proinflammatory cytokines. Consequently, BAY-11-7082 exhibits strong potential as a therapeutic strategy for ameliorating EAN by influencing the balance of M1/M2 macrophages and inflammatory cytokines.

Indexed as

Guillain-Barre SyndromeNeuritis, Autoimmune, ExperimentalAnimalsMacrophagesMaleMiceNitrilesSulfonesTranscription Factor RelA3-(4-methylphenylsulfonyl)-2-propenenitrileNitrilesRela protein, mouseSulfonesTranscription Factor RelABAY11-7082EANGBSmacrophagesNF-κB

Identifiers

PMID34118070
PMCPMC8446411
OpenAlexW3163072238

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.