Evidence map›Paper›PMID 39187319›Full record

ArticleIn vivo (Athens, Greece)

Protective Effects of Imatinib on a DSS-induced Colitis Model Through Regulation of Apoptosis and Inflammation.

Hyeonjin Kim, Chae Yeon Kim, Dongwook Kim, Eungyung Kim, Lei Ma, Kanghyun Park, Zhibin Liu, K E Huang, Weihong Wen, Jiwon Ko and 6 more

Abstract read
In one paragraph

Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. MBNL loss of function in smooth muscle as a model for myotonic dystrophy associated gastrointestinal dysmotility.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Article
  3. Review
  4. 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

16 authors.

Hyeonjin Kim *Department of Animal Science and Biotechnology, Research Institute for Innovative Animal Science, Kyungpook National University, Sangju, Republic of Korea.
Chae Yeon Kim *Department of Animal Science and Biotechnology, Research Institute for Innovative Animal Science, Kyungpook National University, Sangju, Republic of Korea.
Dongwook KimDepartment of Animal Science and Biotechnology, Research Institute for Innovative Animal Science, Kyungpook National University, Sangju, Republic of Korea.
Eungyung KimDepartment of Animal Science and Biotechnology, Research Institute for Innovative Animal Science, Kyungpook National University, Sangju, Republic of Korea.
Lei MaDepartment of Animal Science and Biotechnology, Research Institute for Innovative Animal Science, Kyungpook National University, Sangju, Republic of Korea.
Kanghyun ParkDepartment of Animal Science and Biotechnology, Research Institute for Innovative Animal Science, Kyungpook National University, Sangju, Republic of Korea.
Zhibin LiuDepartment of Animal Science and Biotechnology, Research Institute for Innovative Animal Science, Kyungpook National University, Sangju, Republic of Korea.
K E HuangDepartment of Animal Science and Biotechnology, Research Institute for Innovative Animal Science, Kyungpook National University, Sangju, Republic of Korea.
Weihong WenInstitute of Medical Research, Northwestern Polytechnical University, Xi'an, P.R. China.
Jiwon KoSchool of Life Science and Biotechnology, College of Natural Sciences, Kyungpook National University, Daegu, Republic of Korea.
Su-Geun LimSchool of Life Science and Biotechnology, College of Natural Sciences, Kyungpook National University, Daegu, Republic of Korea.
Younghun SungPreclinical Research Center, Daegu-Gyeongbuk Medical Innovation Foundation (DGMIF), Daegu, Republic of Korea.
Zae Young RyooSchool of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, Republic of Korea.
Jun Koo YiSchool of Animal Life Convergence Science, Hankyong National University, Anseong, Republic of Korea.
Soyoung JangSchool of Life Sciences, BK21 FOUR KNU Creative BioResearch Group, Kyungpook National University, Daegu, Republic of Korea; jangsy@knu.ac.kr.
Myoung Ok KimDepartment of Animal Science and Biotechnology, Research Institute for Innovative Animal Science, Kyungpook National University, Sangju, Republic of Korea; ok4325@knu.ac.kr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimInflammatory bowel disease (IBD) is characterized by dysregulated immune responses and a multifactorial etiology. While imatinib has demonstrated efficacy in the treatment of immune-related diseases, its potential effects in IBD treatment remain underexplored. MATERIALS AND

methodsThis study aimed to investigate the therapeutic effects of imatinib in colitis treatment. A dextran sulfate sodium (DSS)-induced colitis model was used to mimic IBD in mice. Imatinib was administered orally to mice simultaneously with DSS treatment. The effects of imatinib on DSS-induced colitis were evaluated by analyzing colitis-related pathology, including the disease activity index (DAI), histological lesions, inflammatory markers, and tight junction integrity. Additionally, western blot analysis and quantitative real-time polymerase chain reaction were used to assess inflammatory markers, tight-junction proteins, and cell death.

resultsIn the DSS-induced colitis model, imatinib treatment exerted protective effects by attenuating weight loss, restoring colon length, reducing spleen weight, and improving the DAI score and histological lesions. Additionally, imatinib reduced the level of proinflammatory cytokines, including TNF-α, IL-6, and IL-1β. Furthermore, imatinib treatment restored tight-junction integrity and decreased the expression of apoptosis marker proteins.

conclusionOverall, imatinib treatment significantly alleviated the symptoms of DSS-induced colitis by influencing the expression of proinflammatory cytokines, tight junction proteins, and apoptotic markers in mice. These findings highlight imatinib as a potential therapeutic candidate for IBD.

Indexed as

ApoptosisColitisCytokinesDextran SulfateDisease Models, AnimalImatinib MesylateAnimalsBiomarkersInflammationInflammation MediatorsMaleMiceBiomarkersCytokinesDextran SulfateImatinib MesylateInflammation MediatorsapoptosisimatinibinflammationInflammatory bowel diseasetight junction

Identifiers

PMID39187319
PMCPMC11363774

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.