Evidence map›Paper›PMID 29393419›Full record

ArticleMolecular medicine reports2018

HMGB1 mediates microglia activation via the TLR4/NF-κB pathway in coriaria lactone induced epilepsy.

Yunbo Shi, Lingli Zhang, Junfang Teng, Wang Miao

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Meta-analysis of HMGB1 levels in the cerebrospinal fluid and serum of patients with epilepsy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023
    Pooled it
  2. Immune dysregulation and epileptogenesis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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12 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Yunbo Shi *Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
Lingli Zhang *Department of Gastroenterology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
Junfang TengDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
Wang MiaoDepartment of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epilepsy is a chronic and recurrent disease of the central nervous system, with a complex pathology. Recent studies have demonstrated that the activation of glial cells serve an important role in the development of epilepsy. The objective of the present study was to investigate the role of high‑mobility group box‑1 (HMGB1) in mediating the activation of glial cells through the toll‑like receptor 4 (TLR4)/nuclear factor (NF)‑κB signaling pathway in seizure, and the underlying mechanism. The brain tissue of post‑surgery patients with intractable epilepsy after resection and the normal control brain tissue of patients with craniocerebral trauma induced intracranial hypertension were collected. The expression level and distribution pattern of HMGB1, OX42 and NF‑κB p65 were detected by immunohistochemistry. HMGB1, TLR4, receptor for advanced glycation end products (RAGE), NF‑κB p65 and inducible nitric oxide synthase (iNOS) expression levels were detected by western blotting, and serum cytokine levels of interleukin (IL)‑1, IL‑6, tumor necrosis factor (TNF)‑α, transforming growth factor (TGF)‑β and IL‑10 in patients with epilepsy and craniocerebral trauma were detected by ELISA. And cell model of epilepsy was established by coriaria lactone (CL)‑stimulated HM cell, and the same factors were measured. The potential toxic effect of HMGB1 on HM cells was evaluated by MTT and 5‑ethynyl‑2‑deoxyuridine assays. The results demonstrated that compared with the control group, levels of HMGB1, TLR4, RAGE, NF‑κB p65 and iNOS in the brain of the epilepsy group were significantly increased, and increased cytokine levels of IL‑1, IL‑6, TNF‑α, TGF‑β and IL‑10 in patients with epilepsy were also observed. At the same time, the above results were also observed in HM cells stimulated with CL. Overexpression of HMGB1 enhanced the results, while HMGB1 small interfering RNA blocked the function of CL. There was no significant toxic effect of HMGB1 on HM cells. In conclusion, overexpression of HMGB1 potentially promoted epileptogenesis. CL‑induced activation of glial cells may act via up‑regulation of HMGB1 and TLR4/RAGE receptors, and the downstream transcription factor NF‑κB.

Indexed as

Signal TransductionAnimalsBiomarkersBrainCell SurvivalDisease Models, AnimalEpilepsyGene ExpressionHMGB1 ProteinHumansImmunohistochemistryLactonesMicrogliaNF-kappa BToll-Like Receptor 4Biomarkerscoriaria lactoneHMGB1 ProteinLactonesNF-kappa BToll-Like Receptor 4activation of microgliaepilepsyhigh-mobility group box-1nuclear factor-κB p65

Identifiers

PMID29393419
PMCPMC5865977
OpenAlexW2788246607

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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 OpenQuestion graph.