Evidence map›Paper›PMID 30297787›Full record

ArticleScientific reports2018

Transcriptomic analysis reveals a controlling mechanism for NLRP3 and IL-17A in dextran sulfate sodium (DSS)-induced colitis.

Tien-Jen Lin, Shu-Yi Yin, Pei-Wen Hsiao, Ning-Sun Yang, I-Jen Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  3. Article
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  6. Luteolin: A promising natural agent in management of pain in chronic conditions.Frontiers in pain research (Lausanne, Switzerland) · 2023
    Review
  7. Article
  8. Journal of clinical biochemistry and nutrition · 2022
    Article
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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

5 authors at 3 institutions in 1 country.

Tien-Jen LinDepartment of Neurosurgery, Wan Fang Hospital, Taipei Medical University, Taipei, ROC, Taiwan.
Shu-Yi YinAgricultural Biotechnology Research Center, Academia Sinica, Taipei, 115-29, ROC, Taiwan.
Pei-Wen HsiaoAgricultural Biotechnology Research Center, Academia Sinica, Taipei, 115-29, ROC, Taiwan.ORCID http://orcid.org/0000-0002-3589-6754
Ning-Sun YangAgricultural Biotechnology Research Center, Academia Sinica, Taipei, 115-29, ROC, Taiwan.
I-Jen WangDepartment of Pediatrics, Taipei Hospital, Ministry of Health and Welfare, Taipei, Taiwan. wij636@gmail.com.
Agricultural Biotechnology Research Center, Academia Sinica · TWNational Yang Ming Chiao Tung University · TWWan Fang Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The incidence of inflammatory bowel disease (IBD) has markedly increased. Our research findings during the past showed that medicinal plant extracts and the derived phytochemical components from Wedelia chinensis (WC) can have strong anti-colitis activities. Here, we further identified the key component phytochemicals from active fractions of different WC preparations (WCHA) that are responsible for the protective effect of WCHA in colitis mice. Of the 3 major compounds (wedelolactone, luteolin and apigenin) in this fraction, luteolin had the highest anti-inflammatory effect in vivo. Using a next-generation sequencing (NGS) (e.g., RNA-seq) system to analyze the transcriptome of colorectal cells/tissues in mice with dextran sulfate sodium (DSS)-induced colitis with/without phytochemicals treatment, luteolin was found to strongly suppress the DSS-activated IL-17 pathway in colon tissue. In addition, co-treatment with wedelolactone and luteolin had a synergistic effect on the expression level of some IL-17 pathway-related genes. Interestingly, our NGS analyses also indicated that luteolin and wedelolactone can specifically suppress the expression of NLRP3 and NLRP1. Using a 3-dimensional cell co-culture system, we further demonstrated that luteolin could efficiently suppress NLRP3 expression via disruption of IL-17A signaling in inflamed colon tissue, which also indicates the pharmacological potential of luteolin and wedelolactone in treating IBD.

Indexed as

Gene Expression Profiling3T3 CellsAcute DiseaseAlternative SplicingAnimalsColitisColonCoumarinsDextran SulfateFeedback, PhysiologicalInflammasomesInterleukin-17Lipid MetabolismLuteolinMaleMiceCoumarinsDextran SulfateInflammasomesInterleukin-17LuteolinNLR Family, Pyrin Domain-Containing 3 ProteinPhytochemicalsPlant Extractswedelolactone

Identifiers

PMID30297787
PMCPMC6175949
OpenAlexW2895434185

What OpenQuestion holds

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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.