Evidence map›Paper›PMID 26683259›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2016

Novel anti-inflammatory agent 3-[(dodecylthiocarbonyl)-methyl]-glutarimide ameliorates murine models of inflammatory bowel disease.

Nobuki Ichikawa, Kenichiro Yamashita, Tohru Funakoshi, Shin Ichihara, Moto Fukai, Masaomi Ogura, Nozomi Kobayashi, Masaaki Zaitsu, Tadashi Yoshida, Susumu Shibasaki and 8 more

Abstract read
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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 25% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
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

18 authors at 3 institutions in 1 country.

Nobuki IchikawaDepartment of Gastroenterological Surgery I, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan.
Kenichiro YamashitaDepartment of Transplant Surgery, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan. kenchan@med.hokudai.ac.jp.
Tohru FunakoshiDepartment of Gastroenterological Surgery I, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan.
Shin IchiharaDepartment of Surgical Pathology, Sapporo-Kosei General Hospital, N-3, E-8-5, Chuo-ku, Sapporo, 060-0033, Japan.
Moto FukaiDepartment of Transplant Surgery, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan.
Masaomi OguraDepartment of Gastroenterological Surgery I, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan.
Nozomi KobayashiDepartment of Gastroenterological Surgery I, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan.
Masaaki ZaitsuDepartment of Gastroenterological Surgery I, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan.
Tadashi YoshidaDepartment of Gastroenterological Surgery I, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan.
Susumu ShibasakiDepartment of Gastroenterological Surgery I, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan.
Yasuyuki KoshizukaDepartment of Gastroenterological Surgery I, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan.
Yusuke TsunetoshiDepartment of Gastroenterological Surgery I, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan.
Masanori SatoDepartment of Gastroenterological Surgery I, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan.
Takahiro EinamaDepartment of Gastroenterological Surgery I, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan.
Michitaka OzakiFaculty of Health Sciences, School of Medicine, Hokkaido University, N-12, W-5, Kita-ku, Sapporo, 060-0812, Japan.
Kazuo UmezawaDepartment of Molecular Target Medicine, Aichi Medical University, Yazakokarimata 1-1, Nagakute, 480-1195, Japan.
Tomomi SuzukiDepartment of Gastroenterological Surgery I, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan.
Satoru TodoDepartment of Gastroenterological Surgery I, Graduate School of Medicine, Hokkaido University, N-15, W-7, Kita-ku, Sapporo, 060-8638, Japan. s-todo@st-mary-med.or.jp.
Hokkaido University · JPAichi Medical University · JPSapporo Kosei General Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

OBJECTIVE AND

designTo examine the effect of 3-[(dodecylthiocarbonyl)-methyl]-glutarimide (DTCM-G), a novel anti-inflammatory agent that inhibits lipopolysaccharide (LPS) activation of RAW264.7 macrophages, on murine models of colitis and RAW264.7 cells. MATERIALS AND

methodsColitis was induced by rectally infusing trinitrobenzenesulfonic acid (TNBS) (1.5 mg in 50% ethanol) in BALB/c mice or orally administering 3% dextran sulfate sodium (DSS) for 5 days in C57BL/6 mice. The severity of colitis was assessed after intraperitoneally injecting DTCM-G (40 mg/kg). The anti-inflammatory properties of DTCM-G and its mechanisms were investigated in LPS-stimulated RAW264.7 cells.

resultsDTCM-G significantly ameliorated TNBS-induced colitis, according to the body weight loss, disease activity index, colonic obstruction, macroscopic colonic inflammation score, mucosal myeloperoxidase activity, and histopathology. Immunohistochemistry and isolated lamina propria mononuclear cells showed significantly reduced colonic F4/80(+) and CD11b(+) macrophage infiltration. DTCM-G significantly suppressed tumor necrosis factor (TNF)-α and interleukin (IL)-6 messenger RNA expression in the colon and attenuated DSS-induced colitis, according to the disease activity index and histopathology. In RAW264.7 cells, DTCM-G suppressed LPS-induced TNF-α/IL-6 production and enhanced glycogen synthase kinase-3β phosphorylation.

conclusionsDTCM-G attenuated murine experimental colitis by inhibiting macrophage infiltration and inflammatory cytokine expression. Thus, DTCM-G may be a promising treatment for inflammatory bowel disease.

Indexed as

AnimalsAnti-Inflammatory AgentsCD4-Positive T-LymphocytesCell LineColitisColonCytokinesDextran SulfateDisease Models, AnimalMacrophagesMiceMice, Inbred BALB CMice, Inbred C57BLPeroxidasePiperidonesRNA, Messenger3-((dodecylthiocarbonyl)methyl)glutarimideAnti-Inflammatory AgentsCytokinesDextran SulfatePeroxidasePiperidonesRNA, MessengerTrinitrobenzenesulfonic Acid3-[(Dodecylthiocarbonyl)-methyl]-glutarimideColitisDextran sulfate sodiumInflammatory bowel diseaseMacrophageTrinitrobenzenesulfonic acid

Identifiers

PMID26683259
OpenAlexW2300465264

What OpenQuestion holds

Textmetadata
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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.