Evidence map›Paper›PMID 37443707›Full record

ArticleCells2023

Butyrate Protects Myenteric Neurons Loss in Mice Following Experimental Ulcerative Colitis.

Marcos A F Caetano, Henrique I R Magalhães, Jheniffer R L Duarte, Laura B Conceição, Patricia Castelucci

Open access · goldAbstract read
In one paragraph

Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. 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

5 authors at 1 institution in 1 country.

Marcos A F CaetanoDepartment of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo 05508-000, Brazil.ORCID 0000-0002-9981-3241
Henrique I R MagalhãesDepartment of Surgery, School of Veterinary Medicine and Animal Sciences, University of São Paulo, São Paulo 05508-270, Brazil.ORCID 0000-0001-9151-8160
Jheniffer R L DuarteDepartment of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo 05508-000, Brazil.
Laura B ConceiçãoDepartment of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo 05508-000, Brazil.
Patricia CastelucciDepartment of Anatomy, Institute of Biomedical Sciences, University of São Paulo, São Paulo 05508-000, Brazil.
Universidade de São Paulo · BR

Funding

Higher Education Personnel Improvement Coordination 88887.506345/2020-00National Council for Scientific and Technological Development 168015/2018-8Programa Unificado de Bolsas (PUB/USP 736Research Support Foundation of the State of São Paulo 2014/25927-2Research Support Foundation of the State of São Paulo 2018/07862-1Research Support Foundation of the State of São Paulo 2022/04010-0
6 · The paper itself

Abstract

The enteric nervous system is affected by inflammatory bowel diseases (IBD). Gut microbiota ferments dietary fibers and produces short-chain fatty acids, such as Butyrate, which bind to G protein-coupled receptors, such as GPR41, and contribute to maintaining intestinal health. This work aimed to study the GPR41 in myenteric neurons and analyze the effect of Butyrate in mice submitted to experimental ulcerative colitis. The 2, 4, 6 trinitrobenzene sulfonic acid (TNBS) was injected intrarectally in C57BL/6 mice (Colitis). Sham group received ethanol (vehicle). One group was treated with 100 mg/kg of Sodium Butyrate (Butyrate), and the other groups received saline. Animals were euthanized 7 days after colitis induction. Analyzes demonstrated colocalization of GPR41 with neurons immunoreactive (-ir) to nNOS and ChAT-ir and absence of colocalization of the GPR41 with GFAP-ir glia. Quantitative results demonstrated losses of nNOS-ir, ChAT-ir, and GPR41-ir neurons in the Colitis group and Butyrate treatment attenuated neuronal loss. The number of GFAP-ir glia increased in the Colitis group, whereas Butyrate reduced the number of these cells. In addition, morphological alterations observed in the Colitis group were attenuated in the Butyrate group. The presence of GPR41 in myenteric neurons was identified, and the treatment with Butyrate attenuated the damage caused by experimental ulcerative colitis.

Indexed as

ColitisColitis, UlcerativeAnimalsButyric AcidMiceMice, Inbred C57BLNeuronsButyric AcidButyrateenteric nervous systemfree fatty acid receptor 3GPR41gut microbiotainflammatory bowel diseasesshort-chain fatty acids

Identifiers

PMID37443707
PMCPMC10340616
OpenAlexW4381663279

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.