Evidence map›Paper›PMID 26360050›Full record

ArticlePloS one2015

Metformin Ameliorates Inflammatory Bowel Disease by Suppression of the STAT3 Signaling Pathway and Regulation of the between Th17/Treg Balance.

Seon-Yeong Lee, Seung Hoon Lee, Eun-Ji Yang, Eun-Kyung Kim, Jae-Kyung Kim, Dong-Yun Shin, Mi-La Cho

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 1 pooled it
8.2field-weighted citation impact, top 1% 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

127 citing papers in PubMed, 1 synthesis or guideline pooled it, 221 citations in OpenAlex.

  1. Pooled it
  2. Genetic Variants inDiabetes · 2018
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  11. Dysregulated immunometabolism in gut inflammation.Acta biochimica et biophysica Sinica · 2026
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  15. Article
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67 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

7 authors at 2 institutions in 1 country.

Seon-Yeong LeeThe Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea; The Laboratory of Immune Network, CRCID, The Catholic University, Seoul, Republic of Korea.
Seung Hoon LeeThe Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Eun-Ji YangThe Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Eun-Kyung KimThe Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Jae-Kyung KimThe Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea.
Dong-Yun ShinCollege of Pharmacy, Gachon University of Medicine and Science, 191 Hambakmoe-ro, Yeonsu-gu, Incheon 406-799, Korea.
Mi-La ChoThe Rheumatism Research Center, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul, South Korea; The Laboratory of Immune Network, CRCID, The Catholic University, Seoul, Republic of Korea.
Catholic University of Korea · KRGachon University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveMetformin is used to treat type 2 diabetes. We sought to determine whether metformin reduces inflammation, by regulating p-signal transducer and activator of transcription 3 (STAT3) expression and T-helper 17 (Th17) cell proliferation, in a mouse model of inflammatory bowel disease (IBD).

methodsIBD mice were administered metformin for 16 days and their tissues were analyzed. AMP-activated protein kinase (AMPK), the mammalian target of rapamycin (mTOR), p-STAT3 and p-STAT5 in the spleen and lymph nodes were detected using immunohistochemistry and confocal microscopy. Gene expression was determined using quantitative PCR assays, and protein expression levels were measured using western blotting and enzyme-linked immunosorbent assays. Human HT-29 cell proliferation was evaluated using MTT assays.

resultsMetformin reduced disease activity index scores and inhibited weight loss. Metformin also decreased the colonic histological score and inflammatory mediators and increased colon lengths increased. Treatment with metformin inhibited the expression of interleukin (IL)-17, p-STAT3, and p-mTOR. In contrast, metformin treatment increased expression levels of p-AMPK and Foxp3. In addition, expression of inflammatory cytokines decreased in a dose-dependent manner in inflamed human HT-29 cells cultured with metformin at various concentrations.

conclusionsMetformin attenuates IBD severity and reduces inflammation through the inhibition of p-STAT3 and IL-17 expression. Our results have increased our understanding of this chronic inflammatory disease, and support the strategy of using p-STAT3 inhibitors to treat IBD.

Indexed as

AnimalsCell DifferentiationCell LineCytokinesDisease Models, AnimalGene ExpressionHumansInflammation MediatorsInflammatory Bowel DiseasesMetforminMicePhosphorylationRNA, MessengerSignal TransductionSTAT3 Transcription FactorTh17 CellsCytokinesInflammation MediatorsMetforminRNA, MessengerSTAT3 Transcription FactorTOR Serine-Threonine Kinases

Identifiers

PMID26360050
PMCPMC4567351
OpenAlexW1958249906

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.