Evidence map›Paper›PMID 27405597›Full record

ArticleScientific reports2016

Methane limit LPS-induced NF-κB/MAPKs signal in macrophages and suppress immune response in mice by enhancing PI3K/AKT/GSK-3β-mediated IL-10 expression.

Xu Zhang, Na Li, Han Shao, Yan Meng, Liping Wang, Qian Wu, Ying Yao, Jinbao Li, Jinjun Bian, Yan Zhang and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
–field-weighted citation impact
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

45 citing papers in PubMed.

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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

11 authors.

Xu ZhangDepartment of Anesthesiology and Intensive Care, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China (mainland).
Na LiDepartment of Anesthesiology and Intensive Care, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China (mainland).
Han ShaoDepartment of Anesthesiology and Intensive Care, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China (mainland).
Yan MengDepartment of Anesthesiology and Intensive Care, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China (mainland).
Liping WangDepartment of Anesthesiology and Intensive Care, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China (mainland).
Qian WuDepartment of Anesthesiology and Intensive Care, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China (mainland).
Ying YaoDepartment of Anesthesiology and Intensive Care, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China (mainland).
Jinbao LiDepartment of Anesthesiology and Intensive Care, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China (mainland).
Jinjun BianDepartment of Anesthesiology and Intensive Care, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China (mainland).
Yan ZhangDepartment of Anesthesiology and Intensive Care, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China (mainland).
Xiaoming DengDepartment of Anesthesiology and Intensive Care, Changhai Hospital, The Second Military Medical University, Shanghai, 200433, China (mainland).

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory diseases such as sepsis and autoimmune colitis, characterized by an overwhelming activation of the immune system and the counteracting anti-inflammatory response, remain a major health problem in worldwide. Emerging evidence suggests that methane have a protective effect on many animal models, like ischaemia reperfusion injury and diabetes-associated diseases. Whether methane could modulating inflammatory diseases remains largely unknown. Here we show that methane-rich saline (MS) ip treatment (16 ml/kg) alleviated endotoxin shock, bacteria-induced sepsis and dextran-sulfate-sodium-induced colitis in mice via decreased production of TNF-α and IL-6. In MS-treated macrophages, LPS-induced activation of NF-κb/MAPKs was attenuated. Interestingly, MS treatment significantly elevated the levels of IL-10 both in vitro and in vivo. Neutralization of IL-10 abrogated the therapeutic effect of MS. Moreover, anti-IL10 blockade partially restored the MS-mediated attenuation of NF-κb/MAPKs phosphorylation. We further found that MS resulted in markedly enhanced phosphorylation of GSK-3β and AKT, which both mediate the release of Il-10. Additionally, inhibition of PI3K attenuated MS-mediated p-GSK-3β and IL-10 production and reversed the suppressed activation of NF-κb/ MAPKs in response to LPS. Our results reveal a novel effect and mechanisms of methane and support the potential value of MS as a therapeutic approach in innate inflammatory diseases.

Indexed as

AnimalsGlycogen Synthase Kinase 3 betaImmune SystemInterleukin-10LipopolysaccharidesMacrophages, PeritonealMethaneMiceMice, Inbred C57BLMitogen-Activated Protein KinasesNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionToll-Like Receptor 4Glycogen Synthase Kinase 3 betaInterleukin-10LipopolysaccharidesMethaneMitogen-Activated Protein KinasesNF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID27405597
PMCPMC4942692

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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.