Evidence map›Paper›PMID 27900483›Full record

ArticleJournal of gastroenterology2017

Indigo Naturalis ameliorates murine dextran sodium sulfate-induced colitis via aryl hydrocarbon receptor activation.

Shoichiro Kawai, Hideki Iijima, Shinichiro Shinzaki, Satoshi Hiyama, Toshio Yamaguchi, Manabu Araki, Shuko Iwatani, Eri Shiraishi, Akira Mukai, Takahiro Inoue and 6 more

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In one paragraph

Article in Journal of gastroenterology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 6% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

  1. Pooled it
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  15. Pharmaceutical biology · 2024
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9 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

16 authors at 2 institutions in 1 country.

Shoichiro KawaiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Hideki IijimaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan. hiijima@gh.med.osaka-u.ac.jp.
Shinichiro ShinzakiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Satoshi HiyamaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Toshio YamaguchiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Manabu ArakiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Shuko IwataniDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Eri ShiraishiDepartment of Gastroenterology and Hepatology, Sumitomo Hospital, Osaka, Japan.
Akira MukaiDepartment of Gastroenterology and Hepatology, Sumitomo Hospital, Osaka, Japan.
Takahiro InoueDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yoshito HayashiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Masahiko TsujiiDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Daisuke MotookaDepartment of Infection Metagenomics, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Shota NakamuraDepartment of Infection Metagenomics, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Tetsuya IidaDepartment of Infection Metagenomics, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Tetsuo TakeharaDepartment of Gastroenterology and Hepatology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Osaka University · JPSumitomo Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIndigo Naturalis (IN) is used as a traditional herbal medicine for ulcerative colitis (UC). However, the mechanisms of action of IN have not been clarified. We aimed to evaluate the efficacy of IN for ameliorating colonic inflammation. We further investigated the mechanisms of action of IN.

methodsColitis severity was assessed in dextran sodium sulfate-induced colitis and trinitrobenzene sulfonic acid-induced colitis models with or without the oral administration of IN or indigo, which is a known major component of IN. Colonic lamina propria (LP) mononuclear cells isolated from IN-treated mice were analyzed with quantitative reverse transcription polymerase chain reaction (qRT-PCR) and flow cytometry. LP and splenic mononuclear cells cultured in vitro with IN or indigo were also analyzed. The role of the candidate receptor for indigo, the aryl hydrocarbon receptor (AhR), was analyzed using Ahr-deficient mice.

resultsColitis severity was significantly ameliorated in the IN and indigo treatment groups compared with the control group. The mRNA expression levels of interleukin (Il)-10 and Il-22 in the LP lymphocytes were increased by IN treatment. The treatment of splenocytes with IN or indigo increased the expression of anti-inflammatory cytokines and resulted in the expansion of IL-10-producing CD4

conclusionsIN and indigo ameliorated murine colitis through AhR signaling activation, suggesting that AhR could be a promising therapeutic target for UC.

Indexed as

AnimalsCD3 ComplexCD4 Lymphocyte CountCD4-Positive T-LymphocytesCells, CulturedColitisDextran SulfateDrugs, Chinese HerbalFemaleForkhead Transcription FactorsGene ExpressionIndigo CarmineInterleukin-10Interleukin-22Interleukin-2 Receptor alpha SubunitInterleukinsCD3 ComplexDextran SulfateDrugs, Chinese HerbalForkhead Transcription FactorsFoxp3 protein, mouseIl2ra protein, mouseIndigo CarmineInterleukin-10Interleukin-22Interleukin-2 Receptor alpha SubunitInterleukinsNuclear Receptor Subfamily 1, Group F, Member 3Qingdai compoundReceptors, Aryl HydrocarbonRNA, MessengerTrinitrobenzenesulfonic AcidAryl hydrocarbon receptorIndigoIndigo NaturalisInflammatory bowel diseaseUlcerative colitis

Identifiers

PMID27900483
OpenAlexW2558760339

What OpenQuestion holds

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Read underepoch 390

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.