Evidence map›Paper›PMID 31347703›Full record

ArticleBritish journal of pharmacology2019

Butyrate ameliorates caerulein-induced acute pancreatitis and associated intestinal injury by tissue-specific mechanisms.

Xiaohua Pan, Xin Fang, Fei Wang, Hongli Li, Wenying Niu, Wenjie Liang, Chengfei Wu, Jiahong Li, Xing Tu, Li-Long Pan and 1 more

Open access · greenAbstract read
In one paragraph

Article in British journal of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 5 pooled it
13.7field-weighted citation impact, top 1% 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

87 citing papers in PubMed, 5 syntheses or guidelines pooled it, 145 citations in OpenAlex.

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  8. The Roles of Gut Microbiota in the Pathogenesis of Acute Pancreatitis.Medical science monitor : international medical journal of experimental and clinical research · 2026
    Review
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27 more citing papers are in PubMed but not listed here.

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

11 authors at 2 institutions in 1 country.

Xiaohua PanState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.
Xin FangState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.
Fei WangDivision of Gastroenterology and Hepatology, Digestive Disease Institute, Tongji Hospital, Tongji University School of Medicine, Shanghai, China.
Hongli LiState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.
Wenying NiuState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.
Wenjie LiangState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.
Chengfei WuState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.
Jiahong LiState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.
Xing TuState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.
Li-Long PanSchool of Medicine, Jiangnan University, Wuxi, China.
Jia SunState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi, China.ORCID 0000-0002-4874-1305
Jiangnan University · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeAcute pancreatitis (AP) is a common acute abdominal condition, frequently associated with intestinal barrier dysfunction, which aggravates AP retroactively. Butyrate exhibits anti-inflammatory effects in a variety of inflammatory diseases. However, its potential beneficial effect on AP and the underlying mechanisms have not been investigated. EXPERIMENTAL APPROACH: Experimental AP was induced by caerulein hyperstimulation in wild-type and GPR109A KEY

resultsButyrate prophylaxis attenuated AP as shown by reduced serum amylase and lipase levels, pancreatic oedema, myeloperoxidase activity, and improved pancreatic morphology. Amelioration of pancreatic damage by butyrate was associated with reduced levels of TNF-α, IL-6, and CCL2 and suppressed activation of the NLRP3 inflammasome in both pancreas and colon. Further, butyrate ameliorated pancreatic inflammation by suppressing interactions between histone deacetylase 1 (HDAC1) and AP1 and STAT1 with increased histone acetylation at H3K9, H3K14, H3K18, and H3K27 loci, resulting in suppression of NLRP3 inflammasome activation and modulation of immune cell infiltration in pancreas. Additionally, butyrate mediated STAT1/AP1-NLRP3 inflammasome suppression via HDAC1 inhibition was demonstrated in peritoneal macrophage. In colon, butyrate inhibited NLRP3 inflammasome activation via GPR109A. Accordingly, the modulatory effects of butyrate on AP, AP-associated gut dysfunction, and NLRP3 inflammasome activation were diminished in GPR109A CONCLUSION AND IMPLICATIONS: Our study dissected tissue-specific anti-inflammatory mechanisms of butyrate during AP, suggesting that increased colonic levels of butyrate may be a strategy to protect against AP.

Indexed as

Acute DiseaseAdministration, OralAnimalsAnti-Inflammatory Agents, Non-SteroidalButyratesCeruletideFemaleIntestinal DiseasesIntestine, SmallMacrophagesMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutPancreasPancreatitisAnti-Inflammatory Agents, Non-SteroidalButyratesCeruletide

Identifiers

PMID31347703
PMCPMC6932943
OpenAlexW2965295305

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.