Evidence map›Paper›PMID 41379810›Full record

ArticlePloS one2025

Butyrate ameliorates DSS-induced ulcerative colitis in mice by facilitating autophagy in intestinal epithelial cells and modulating the gut microbiota through blocking the PI3K-AKT-mTOR pathway.

Ruifang Li, Yan Sun, Drolma Kelsang, Mingzhi Feng, Hanhui Cai, Jun Zhang

Abstract read
In one paragraph

Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 2 pooled it
–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, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
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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.

Ruifang LiCenter for General Practice Medicine, Department of Gastroenterology, Zhejiang Provincial People's Hospital, (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, Zhejiang, P.R China.
Yan SunCenter for General Practice Medicine, Department of Gastroenterology, Zhejiang Provincial People's Hospital, (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, Zhejiang, P.R China.
Drolma KelsangCenter for General Practice Medicine, Department of Gastroenterology, Zhejiang Provincial People's Hospital, (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, Zhejiang, P.R China.
Mingzhi FengCenter for General Practice Medicine, Department of Gastroenterology, Zhejiang Provincial People's Hospital, (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, Zhejiang, P.R China.
Hanhui CaiEmergency and Critical Care Center, Intensive Care Unit, Zhejiang Provincial People's Hospital, (Affiliated People's Hospital, Hangzhou Medical College), Hangzhou, Zhejiang, P.R China.
Jun ZhangDepartment of Gastroenterology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Traditional Chinese Medicine), Hangzhou, Zhejiang, P.R China.ORCID https://orcid.org/0000-0003-3618-1723

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUlcerative colitis (UC) is an idiopathic, chronic inflammatory disease of the colon that imposes a significant global public health burden due to its recurrent and refractory nature. The therapeutic effects of butyrate on UC have been documented previously, but its specific mechanisms remain unclear.

objectiveThis study aimed to investigate the effects and potential mechanisms of butyrate in dextran sulfate sodium (DSS)-induced UC.

methodsA UC mouse model was induced utilizing 3% DSS, followed by interventions of 300 mg/kg, 600 mg/kg, or 1200 mg/kg of butyrate. The fecal condition and colonic pathology of the mice were observed, along with measurements of body weight and colon length. The expression of serum inflammatory factors, autophagy-related proteins, and the PI3K/AKT/mTOR pathway-related proteins were detected. Additionally, the impact of butyrate on the mouse gut microbial communities was evaluated using 16S rRNA sequencing technology.

resultsIt was demonstrated that butyrate effectively alleviated UC symptoms, including bloody stools, weight loss, and colon shortening. Furthermore, butyrate reduced colonic tissue damage, decreased the expression of TNF-α, IL-1β, and IL-6, and significantly upregulated Beclin-1, Atg5, and the LC3II/I ratio, while reducing P62 expression. Butyrate also decreased the relative expression of p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR. 16S rRNA sequencing results revealed that butyrate improved the intestinal microbial community structure by inhibiting harmful bacteria and accelerating the growth of beneficial bacteria.

conclusionThis study suggests that butyrate may alleviate DSS-induced UC in mice by blocking the PI3K/AKT/mTOR pathway to facilitating autophagy in intestinal epithelial cells and by modulating the gut microbiota.

Indexed as

AutophagyButyratesColitis, UlcerativeGastrointestinal MicrobiomeAnimalsDextran SulfateDisease Models, AnimalEpithelial CellsIntestinal MucosaMaleMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesButyratesDextran SulfatemTOR protein, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinases

Identifiers

PMID41379810
PMCPMC12697976

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.