Evidence map›Paper›PMID 40065908›Full record

ArticleJournal of inflammation research2025

Lijiao Yang, Wanyu Li, Qianjing Zhao, Qi Mo, Tianyu Liu, Hailong Cao

Abstract read
In one paragraph

Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Frontiers in immunology · 2026
    Article
  5. Review
  6. Pharmaceuticals (Basel, Switzerland) · 2025
    Article
  7. 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

6 authors.

Lijiao Yang *Department of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, National Key Clinical Specialty, Tianjin Institute of Digestive Diseases, Tianjin Key Laboratory of Digestive Diseases, Tianjin, 300052, People's Republic of China.
Wanyu Li *Department of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, National Key Clinical Specialty, Tianjin Institute of Digestive Diseases, Tianjin Key Laboratory of Digestive Diseases, Tianjin, 300052, People's Republic of China.
Qianjing Zhao *Department of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, National Key Clinical Specialty, Tianjin Institute of Digestive Diseases, Tianjin Key Laboratory of Digestive Diseases, Tianjin, 300052, People's Republic of China.
Qi MoDepartment of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, National Key Clinical Specialty, Tianjin Institute of Digestive Diseases, Tianjin Key Laboratory of Digestive Diseases, Tianjin, 300052, People's Republic of China.
Tianyu LiuDepartment of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, National Key Clinical Specialty, Tianjin Institute of Digestive Diseases, Tianjin Key Laboratory of Digestive Diseases, Tianjin, 300052, People's Republic of China.
Hailong CaoDepartment of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, National Key Clinical Specialty, Tianjin Institute of Digestive Diseases, Tianjin Key Laboratory of Digestive Diseases, Tianjin, 300052, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Ulcerative colitis (UC), a typical inflammatory bowel disease (IBD), is pathologically defined by mucosal inflammation confined to the colonic mucosa. Methods: A murine model of colitis was established through administration of dextran sulfate sodium (DSS), followed by oral gavage with either SbS or the control Sabouraud dextrose broth (SDB) culture medium. The FXR activation, NLRP3 inflammasome inhibition, and macrophage pyroptosis were evaluated both in vivo and in vitro. The effects of SbS in activating FXR, suppressing NLRP3 inflammasome and alleviating the colitis were assessed. Results: SbS ameliorated symptoms of DSS-induced colitis. Our data demonstrated that SbS elicited activation of FXR and concomitantly suppressed NLRP3 expression within the colonic tissue samples. Additionally, SbS was further observed to suppress the expression of cleaved caspase-1, a key effector protein in pyroptosis process, within the F4/80 Conclusion: SbS demonstrated a beneficial effect in alleviating UC by modulating the FXR-NLRP3 signaling pathway, thereby mitigating macrophage pyroptosis. This discovery presents new insights into effects of Sb on alleviating UC.

Indexed as

colitisFarnesoid X receptormacrophagesNLRP3 inflammasomepyroptosisSaccharomyces boulardii

Identifiers

PMID40065908
PMCPMC11891491

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.