Evidence map›Paper›PMID 39991681›Full record

ArticleWorld journal of gastroenterology2025

Mesalazine alleviated the symptoms of spontaneous colitis in interleukin-10 knockout mice by regulating the STAT3/NF-κB signaling pathway.

Qian Chen, Ya-Li Zhang, Yong-Quan Shi, Lie Zheng

Abstract read
In one paragraph

Article in World journal of gastroenterology, 2025. 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
–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

2 citing papers in PubMed.

  1. Article
  2. Review
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

4 authors.

Qian ChenInstitute of Digestive Disease, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.
Ya-Li ZhangInstitute of Digestive Disease, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China.
Yong-Quan ShiDepartment of Gastroenterology, Xijing Hospital affiliated to Air Force Medical University, Xi'an 710032, Shaanxi Province, China.
Lie ZhengDepartment of Gastroenterology, Traditional Chinese Medicine Hospital of Shaanxi Province, Xi'an 710003, Shaanxi Province, China. 492688049@qq.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExcessive endoplasmic reticulum (ER) stress in intestinal epithelial cells can lead to damage to the intestinal mucosal barrier, activate the signal transducer and activator of transcription 3 (STAT3)/nuclear factor kappa B (NF-κB) signaling pathway, and exacerbate the inflammatory response, thus participating in the pathogenesis of ulcerative colitis (UC). Mesalazine is a commonly used drug in the clinical treatment of UC. However, further studies are needed to determine whether mesalazine regulates the ER stress of intestinal epithelial cells, down-regulates the STAT3/NF-κB pathway to play a role in the treatment of UC.

aimTo study the therapeutic effects of mesalazine on spontaneous colitis in interleukin-10 (IL-10)

methodsThe 24-week-old IL-10

resultsMesalazine reduced the symptoms of spontaneous colitis in IL-10 knockout mice and the histopathological damage of colonic tissues, and alleviated the ER stress in epithelial cells of colitis mice. Western blotting and quantitative real-time polymerase chain reaction results showed that the STAT3/NF-κB pathway in the colon tissue of model mice was activated, suggesting that this pathway was involved in the pathogenesis of UC and might become a potential therapeutic target. Mesalazine could down-regulate the protein expressions of p-STAT3, NF-κB and p-IκB, and down-regulate the mRNA expression of STAT3 and NF-κB.

conclusionMesalazine may play a protective role in UC by reducing ER stress by regulating the STAT3/NF-κB signaling pathway.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalColitis, UlcerativeInterleukin-10MesalamineNF-kappa BSTAT3 Transcription FactorAnimalsColonDisease Models, AnimalEndoplasmic Reticulum StressFemaleIntestinal MucosaMaleMiceMice, Inbred C57BLMice, KnockoutAnti-Inflammatory Agents, Non-SteroidalIL10 protein, mouseInterleukin-10MesalamineNF-kappa BStat3 protein, mouseSTAT3 Transcription FactorEndoplasmic reticulum stressInflammatory bowel diseaseInterleukin-10-/- miceMesalazineSignal transducer and activator of transcription 3/nuclear factor kappa B signaling pathwayUlcerative colitis

Identifiers

PMID39991681
PMCPMC11755248

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.