Evidence map›Paper›PMID 26464648›Full record

ArticleInternational journal of clinical and experimental pathology2015

Endotoxin tolerance alleviates experimental acute liver failure via inhibition of high mobility group box 1.

Nai-Bin Yang, Shun-Lan Ni, Shan-Shan Li, Sai-Nan Zhang, Dan-Ping Hu, Ming-Qin Lu

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Nai-Bin YangDepartment of Infection Diseases, The First Affiliated Hospital of Wenzhou Medical University Wenzhou 325000, Zhejiang, P. R. China ; Wenzhou Key Laboratory of Hepatology Wenzhou 325000, Zhejiang, P. R. China ; Hepatology Institute of Wenzhou Medical University Wenzhou 325000, Zhejiang, P. R. China.
Shun-Lan NiDepartment of Infection Diseases, The First Affiliated Hospital of Wenzhou Medical University Wenzhou 325000, Zhejiang, P. R. China ; Wenzhou Key Laboratory of Hepatology Wenzhou 325000, Zhejiang, P. R. China ; Hepatology Institute of Wenzhou Medical University Wenzhou 325000, Zhejiang, P. R. China.
Shan-Shan LiDepartment of Infection Diseases, The First Affiliated Hospital of Wenzhou Medical University Wenzhou 325000, Zhejiang, P. R. China ; Wenzhou Key Laboratory of Hepatology Wenzhou 325000, Zhejiang, P. R. China ; Hepatology Institute of Wenzhou Medical University Wenzhou 325000, Zhejiang, P. R. China.
Sai-Nan ZhangDepartment of Infection Diseases, The First Affiliated Hospital of Wenzhou Medical University Wenzhou 325000, Zhejiang, P. R. China ; Wenzhou Key Laboratory of Hepatology Wenzhou 325000, Zhejiang, P. R. China ; Hepatology Institute of Wenzhou Medical University Wenzhou 325000, Zhejiang, P. R. China.
Dan-Ping HuDepartment of Infectious Diseases, The Third Affiliated Hospital of Wenzhou Medical University 108 Wansong Road, Ruian 325200, Zhejiang, China.
Ming-Qin LuDepartment of Infection Diseases, The First Affiliated Hospital of Wenzhou Medical University Wenzhou 325000, Zhejiang, P. R. China ; Wenzhou Key Laboratory of Hepatology Wenzhou 325000, Zhejiang, P. R. China ; Hepatology Institute of Wenzhou Medical University Wenzhou 325000, Zhejiang, P. R. China.
Wenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High mobility group box 1 (HMGB1) has been widely reported to mediate damage caused by inflammatory responses. The aim of our study is to investigate the role of HMGB1 in endotoxin tolerance (ET) alleviating inflammation of acute liver failure (ALF) rats and its possible signaling mechanism. To mimic ET, male Sprague-Dawley rats were pretreated with low dose of lipopolysaccharide (LPS) (0.1 mg/kg once a day intraperitoneally for consecutive five days) before subsequent ALF induction. ALF was induced by intraperitoneal administration of D-GalN/LPS. ET induced by LPS pretreatment significantly improved the survival rate of ALF rats. Moreover, after ALF induction, ET+ALF rats exhibited lower serum enzyme (ALT, AST and TBiL) levels, lower production of inflammatory cytokines (IL-6, TNF-a and HMGB1) and more minor liver histopathological damage than ALF rats. ET+ALF rats showed enhanced expression levels of HMGB1, decreased levels of STAT1 and p-STAT1, augmented expression of SOCS1 in liver tissues than ALF rats. These results indicated that ET induced by low-dose LPS pretreatment may alleviate inflammation and liver injury in experimental acute liver failure rats mainly through inhibition of hepatic HMGB1 translocation and release.

Indexed as

Drug ToleranceLipopolysaccharidesAnimalsDisease Models, AnimalHMGB1 ProteinInterleukin-6LiverLiver Failure, AcuteMalePhosphorylationRatsRats, Sprague-DawleySignal TransductionSTAT1 Transcription FactorTumor Necrosis Factor-alphaHMGB1 ProteinInterleukin-6LipopolysaccharidesSTAT1 Transcription FactorTumor Necrosis Factor-alphaacute liver failureEndotoxin tolerancehigh mobility group box 1JAK/STAT1 signalinglipopolysaccharide (LPS)

Identifiers

PMID26464648
PMCPMC4583880
OpenAlexW1943576048

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.