Evidence map›Paper›PMID 30143931›Full record

ArticleInflammation2018

Arctigenin Ameliorates Inflammation by Regulating Accumulation and Functional Activity of MDSCs in Endotoxin Shock.

Hui Shi, Guanjun Dong, Fenglian Yan, Hui Zhang, Chunxia Li, Qun Ma, Junfeng Zhang, Zhaochen Ning, Zhihua Li, Jun Dai and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 17 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

14 authors at 3 institutions in 2 countries.

Hui ShiInstitute of Immunology and Molecular Medicine, Jining Medical University, Shandong, 272067, China.
Guanjun DongInstitute of Immunology and Molecular Medicine, Jining Medical University, Shandong, 272067, China.
Fenglian YanInstitute of Immunology and Molecular Medicine, Jining Medical University, Shandong, 272067, China.
Hui ZhangInstitute of Immunology and Molecular Medicine, Jining Medical University, Shandong, 272067, China.
Chunxia LiInstitute of Immunology and Molecular Medicine, Jining Medical University, Shandong, 272067, China.
Qun MaInstitute of Immunology and Molecular Medicine, Jining Medical University, Shandong, 272067, China.
Junfeng ZhangInstitute of Immunology and Molecular Medicine, Jining Medical University, Shandong, 272067, China.
Zhaochen NingInstitute of Immunology and Molecular Medicine, Jining Medical University, Shandong, 272067, China.
Zhihua LiInstitute of Immunology and Molecular Medicine, Jining Medical University, Shandong, 272067, China.
Jun DaiInstitute of Immunology and Molecular Medicine, Jining Medical University, Shandong, 272067, China.
Jiankuo MingInstitute of Immunology and Molecular Medicine, Jining Medical University, Shandong, 272067, China.
Runping FangState Key Laboratory of Medicinal Chemical Biology, Department of Biochemistry, College of Life Sciences, Nankai University, Tianjin, 300071, People's Republic of China.
Chuanping SiInstitute of Immunology and Molecular Medicine, Jining Medical University, Shandong, 272067, China.
Huabao XiongInstitute of Immunology and Molecular Medicine, Jining Medical University, Shandong, 272067, China. huabao.xiong@mssm.edu.
Jining Medical University · CNIcahn School of Medicine at Mount Sinai · USNankai University · CN

Funding

Natural Science Foundation of Shandong Province NO. ZR2017BH016Natural Science Foundation of Shandong Province NO. ZR2017BH057Projects of Jining Medical University JY2017KJ009Projects of Science and Technology in Shandong Province NO. J17KA230
6 · The paper itself

Abstract

Endotoxin shock is a life-threatening response caused by a disordered immune response to an infection. MDSCs are accumulated and play a protective role in the pathogenesis of endotoxin shock. However, the regulation of MDSCs by small molecule remains unrevealed. Here, we report that arctigenin, a small molecule extracted from Arctium lappa, induces accumulation of functional MDSCs. Arctigenin was able to ameliorate LPS-induced inflammation through accumulating MDSCs, especially granulocytic MDSCs (G-MDSCs), and enhancing the immunosuppressive function of MDSCs in vivo and in vitro. Mechanistically, arctigenin promoted the accumulation of MDSCs through upregulating miR-127-5p which targets the 3'UTR of interferon regulatory factor-8 (IRF8) mRNA. In addition, arctigenin enhanced the immunosuppressive activity of MDSCs on M1 macrophage polarization by elevating the expression of arginase 1 (Arg-1) and inducible nitric oxide synthase (iNOS). Our study provides new insights into the regulation of functional MDSCs by arctigenin in exerting immune responses and pathogenesis of inflammatory diseases.

Indexed as

AnimalsArginaseFuransInflammationInterferon Regulatory Factor-8Interferon Regulatory FactorsLignansLipopolysaccharidesMiceMicroRNAsMyeloid-Derived Suppressor CellsNitric Oxide Synthase Type IIRNA, MessengerShock, SepticarctigeninArg1 protein, mouseArginaseFuransInterferon Regulatory Factor-8Interferon Regulatory FactorsLignansLipopolysaccharidesMicroRNAsMirn127 microRNA, mouseNitric Oxide Synthase Type IINos2 protein, mouseRNA, MessengerarctigeninArg-1iNOSIRF8LPSMDSCs

Identifiers

PMID30143931
OpenAlexW2888499920

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.