Evidence map›Paper›PMID 30903547›Full record

ArticleInflammation2019

Sodium Butyrate Ameliorates Intestinal Injury and Improves Survival in a Rat Model of Cecal Ligation and Puncture-Induced Sepsis.

Jiahong Fu, Guofu Li, Xingmao Wu, Bin Zang

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.7field-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

35 citing papers in PubMed, 52 citations in OpenAlex.

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  15. Claudin-2 upregulation enhances intestinal permeability, immune activation, dysbiosis, and mortality in sepsis.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  16. Effects ofNutrients · 2024
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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

4 authors at 1 institution in 1 country.

Jiahong FuDepartment of Critical Care Medicine, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning Province, China.
Guofu LiDepartment of Critical Care Medicine, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning Province, China.
Xingmao WuDepartment of Critical Care Medicine, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning Province, China.
Bin ZangDepartment of Critical Care Medicine, Shengjing Hospital of China Medical University, No. 36 Sanhao Street, Heping District, Shenyang, 110004, Liaoning Province, China. zangb@sj-hospital.org.ORCID http://orcid.org/0000-0002-2734-9590
China Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is a life-threatening condition with a high rate of mortality. Unfortunately, very few therapies can improve outcomes in patients with sepsis. Butyrate, which is the most potent histone deacetylase (HDAC) inhibitor among short-chain fatty acids, exerts anti-inflammatory effects in a variety of inflammatory diseases. Butyrate might thus be valuable in the treatment of sepsis, in which inhibition of overwhelming cytokine release is vitally important. Sepsis was induced in 7- to 8-week-old Sprague-Dawley rats by cecal ligation and puncture (CLP) with a 21-g double-puncture technique. Rats received an intravenous injection of normal saline (vehicle) or sodium butyrate (200 mg/kg) after CLP and were sacrificed 12 h later. Hematoxylin and eosin staining was performed to observe the intestinal mucosal morphology. RT-PCR and ELISA were used to determine the intestinal inflammatory response in vivo. Intestinal permeability was evaluated by measuring fluorescein isothiocyanate dextran (FD-4) absorption in vivo, and tight junction protein expression was examined by western blot. NF-κB p65 activities were assessed by western blot and immunohistochemistry. Sodium butyrate treatment improved the survival rate of CLP rats and alleviated sepsis-induced intestinal mucosal injury. Proinflammatory cytokine expression was lower in butyrate-treated rats than in the vehicle group. FD-4 leakage from the intestinal tract was reduced, and the expression levels of the tight junction proteins claudin-1 and ZO-1 were also restored in rats that received sodium butyrate treatment. These effects were associated with less NF-κB p65 nuclear translocation, whereas the expression of Iκ-Bα was not affected or even increased. Sodium butyrate mitigates the inflammatory response and maintains intestinal barrier function in polymicrobial sepsis partly through inhibition of NF-κB activation and may serve as a novel therapy for sepsis.

Indexed as

AnimalsButyric AcidCecumInflammationIntestinal MucosaIntestinesLigationNF-kappa BPuncturesRatsSepsisSurvival RateButyric AcidNF-kappa Bbutyrateintestinal injuryNF-kappa Bsepsis

Identifiers

PMID30903547
OpenAlexW2939471749

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.