Evidence map›Paper›PMID 28754974›Full record

ArticleScientific reports2017

Blockade of high-mobility group box 1 attenuates intestinal mucosal barrier dysfunction in experimental acute pancreatitis.

Xia Chen, Hong-Xian Zhao, Chao Bai, Xiang-Yu Zhou

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. HMGB1: key mediator in digestive system diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
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  18. High-mobility group box-1 inhibition stabilizes intestinal permeability through tight junctions in experimental acute necrotizing pancreatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019
    Article
  19. 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

4 authors at 2 institutions in 1 country.

Xia ChenDepartment of Gastroenterology, The Affiliated Hospital of Southwest Medical University, Luzhou City, P.R. China, 646000. 970217858@qq.com.
Hong-Xian ZhaoDepartment of Histology and Embryology, Southwest Medical University, Luzhou City, P.R. China, 646000.
Chao BaiDepartment of Gastroenterology, The Affiliated Hospital of Southwest Medical University, Luzhou City, P.R. China, 646000.
Xiang-Yu ZhouDepartment of Vascular and Thyroid surgery, The Affiliated Hospital of Southwest Medical University, Luzhou City, P. R. China, 646000.
Affiliated Hospital of Southwest Medical University · CNSouthwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The release of inflammatory cytokines, that plays a dominant role in local pancreatic inflammation and systemic complications in severe acute pancreatitis (SAP). High-mobility group box 1 (HMGB1) is implicated in the mechanism of organ dysfunction and bacterial translocation in SAP. This current study aims to investigate possible role of HMGB1 in the intestinal mucosal barrier dysfunction of SAP, and the effect of anti-HMGB1 antibody treatment in intestinal mucosal injury in SAP. Our data revealed that the HMGB1 expression was significantly increased in AP mice induced by caerulein and LPS, and the inhibition of HMGB1 played a protective role in intestinal mucosal barrier dysfunction, reduced the serum level of other proinflammatory cytokines include IL-1β, IL-6, TNF-α. Next we investigated the downstream receptors involving in HMGB1 signaling. We found that the expressions of toll-like receptor (TLR) 4 and TLR9 were elevated in ileum of AP mice, the administration of HMGB1 neutralizing antibody significantly reduced the TLR4 and TLR9 expression. It was concluded that HMGB1 contributed the mechanism to the intestinal mucosal barrier dysfunction during AP. Blockade of HMGB1 by administration of HMGB1 neutralizing antibody may be a beneficial therapeutic strategy in improving intestinal mucosal barrier dysfunction in SAP.

Indexed as

AnimalsAntibodies, NeutralizingCeruletideHMGB1 ProteinInterleukin-1betaInterleukin-6Intestinal MucosaLipopolysaccharidesMaleMicePancreatitis, Acute NecrotizingToll-Like Receptor 4Toll-Like Receptor 9Tumor Necrosis Factor-alphaAntibodies, NeutralizingCeruletideHMGB1 ProteinHMGB1 protein, mouseInterleukin-1betaInterleukin-6LipopolysaccharidesTlr4 protein, mouseTlr9 protein, mouseToll-Like Receptor 4Toll-Like Receptor 9Tumor Necrosis Factor-alpha

Identifiers

PMID28754974
PMCPMC5533736
OpenAlexW2737498435

What OpenQuestion holds

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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.