Evidence map›Paper›PMID 38159175›Full record

ArticleInflammation2024

Sodium Butyrate Ameliorates Atopic Dermatitis-Induced Inflammation by Inhibiting HDAC3-Mediated STAT1 and NF-κB Pathway.

Chaoqun Hu, Dan Zeng, Yunxia Huang, Qian Deng, Shunan Liu, Weikang Zhou, Wei Zhou

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

22 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Butyrate Is Associated with the Antidepressant Effects ofInternational journal of molecular sciences · 2026
    Article
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  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. ButyrylatedActa pharmaceutica Sinica. B · 2025
    Article
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  11. Review
  12. 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

7 authors at 2 institutions in 1 country.

Chaoqun HuDepartment of Gastroenterology, Chongqing General Hospital, Chongqing, 400014, China.
Dan ZengDepartment of Allergy, Chongqing General Hospital, Chongqing, 400014, China.
Yunxia HuangDepartment of Dermatology, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Qian DengDepartment of Gastroenterology, Chongqing General Hospital, Chongqing, 400014, China.
Shunan LiuDepartment of Dermatology, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Weikang ZhouDepartment of Allergy, Chongqing General Hospital, Chongqing, 400014, China.
Wei ZhouDepartment of Allergy, Chongqing General Hospital, Chongqing, 400014, China. zw_fortomorrow@163.com.
First People's Hospital of Chongqing · CNAffiliated Hospital of Southwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A topic dermatitis (AD) is a common chronic and recurrent skin disorder. The protective effects of sodium butyrate (NaB), a metabolite of short-chain fatty acid breakdown by the gut microbiota, have been widely reported in numerous inflammatory diseases. However, the effect of NaB treatment alone on AD has not been reported. In the current study, AD was induced in BALB/c mice with 2,4-dinitrochlorobenzene (DNCB) for 28 days with NaB (200 mg/kg) treatment by gavage. NaB attenuated AD-induced skin bleeding, scarring, dryness, abrasions and erosions. In addition, NaB inhibited inflammatory cells infiltration and attenuated the expression of inflammatory cytokines and chemokines. Mechanistically, NaB reduced histone deacetylase 3 (HDAC3) expression and NF-κB p65 nuclear translocation by increasing the lysine acetylation levels of STAT1 and NF-κB p65 in AD. Taken together, our study suggests that NaB inhibits inflammatory mediators and ameliorates AD by inhibiting HDAC3 expression, thereby upregulating STAT1 and NF-κB p65 lysine acetylation levels and reducing NF-κB p65 nuclear translocation. Therefore, this study provides a new theoretical basis for NaB in the treatment of AD.

Indexed as

Butyric AcidDermatitis, AtopicHistone DeacetylasesInflammationMice, Inbred BALB CNF-kappa BSTAT1 Transcription FactorAnimalsHistone Deacetylase 3MiceSignal TransductionTranscription Factor RelAButyric AcidHistone Deacetylase 3Histone DeacetylasesNF-kappa BStat1 protein, mouseSTAT1 Transcription FactorTranscription Factor RelAatopic dermatitisHDAC3inflammation.NF-κBsodium butyrate

Identifiers

PMID38159175
OpenAlexW4390441249

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.