Evidence map›Paper›PMID 28528363›Full record

ArticleInflammopharmacology2018

Caffeic acid phenethyl ester is protective in experimental ulcerative colitis via reduction in levels of pro-inflammatory mediators and enhancement of epithelial barrier function.

Mohammed N Khan, Majella E Lane, Paul A McCarron, Murtaza M Tambuwala

Open access · hybridAbstract read
In one paragraph

Article in Inflammopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
5.1field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 62 citations in OpenAlex.

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  14. Anethole Ameliorates Acetic Acid-Induced Colitis in Mice: Anti-Inflammatory and Antioxidant Effects.Evidence-based complementary and alternative medicine : eCAM · 2022
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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 2 institutions in 1 country.

Mohammed N KhanSAAD Centre for Pharmacy and Diabetes, School of Pharmacy and Pharmaceutical Science, Ulster University, Coleraine, County Londonderry, BT52 1SA, Northern Ireland, UK.
Majella E LaneUCL School of Pharmacy, 29-39 Brunswick Square, London, WC1N 1AX, UK.
Paul A McCarronSAAD Centre for Pharmacy and Diabetes, School of Pharmacy and Pharmaceutical Science, Ulster University, Coleraine, County Londonderry, BT52 1SA, Northern Ireland, UK.
Murtaza M TambuwalaSAAD Centre for Pharmacy and Diabetes, School of Pharmacy and Pharmaceutical Science, Ulster University, Coleraine, County Londonderry, BT52 1SA, Northern Ireland, UK. m.tambuwala@ulster.ac.uk.
University of Ulster · GBUniversity College London · GB

Funding

University of Ulster RCF 2014
6 · The paper itself

Abstract

backgroundInhibition of the nuclear factor kappa beta (NF-κβ) pathway has been proposed as a therapeutic target due to its key role in the expression of pro-inflammatory genes, including pro-inflammatory cytokines, chemokines, and adhesion molecules. Caffeic acid phenethyl ester (CAPE) is a naturally occurring anti-inflammatory agent, found in propolis, and has been reported as a specific inhibitor of NF-κβ. However, the impact of CAPE on levels of myeloperoxidases (MPO) and pro-inflammatory cytokines during inflammation is not clear. The aims of this study were to investigate the protective efficacy of CAPE in the mouse model of colitis and determine its effect on MPO activity, pro-inflammatory cytokines levels, and intestinal permeability.

methodDextran sulphate sodium was administered in drinking water to induce colitis in C57/BL6 mice before treatment with intraperitoneal administration of CAPE (30 mg kg

resultsCAPE-treated mice had lower DAI and tissue inflammation scores, with improved epithelial barrier protection and significant reduction in the level of MPO and pro-inflammatory cytokines.

conclusionOur results show that CAPE is effective in suppressing inflammation-triggered MPO activity and pro-inflammatory cytokines production while enhancing epithelial barrier function in experimental colitis. Thus, we conclude that CAPE could be a potential therapeutic agent for further clinical investigations for treatment of inflammatory bowel diseases in humans.

Indexed as

AnimalsAnti-Inflammatory AgentsCaffeic AcidsColitis, UlcerativeCytokinesDextran SulfateDisease Models, AnimalEpithelial CellsFemaleInflammationInflammation MediatorsMice, Inbred C57BLNF-kappa BPhenylethyl AlcoholProtective AgentsAnti-Inflammatory Agentscaffeic acid phenethyl esterCaffeic AcidsCytokinesDextran SulfateInflammation MediatorsNF-kappa BPhenylethyl AlcoholProtective AgentsColitisInflammatory bowel diseasesIntestinal permeabilityNaturalNuclear factor kappa betaPro-inflammatory cytokines

Identifiers

PMID28528363
PMCPMC5859149
OpenAlexW2614299446

What OpenQuestion holds

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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 OpenQuestion graph.