Evidence map›Paper›PMID 27981377›Full record

ArticleInternational journal of colorectal disease2017

Myrrh exerts barrier-stabilising and -protective effects in HT-29/B6 and Caco-2 intestinal epithelial cells.

Rita Rosenthal, Julia Luettig, Nina A Hering, Susanne M Krug, Uwe Albrecht, Michael Fromm, Jörg-Dieter Schulzke

Abstract read
PubMed Publisher
In one paragraph

Article in International journal of colorectal disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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  12. Contribution ofFrontiers in microbiology · 2020
    Article
  13. Curcumin Mitigates Immune-Induced Epithelial Barrier Dysfunction byInternational journal of molecular sciences · 2019
    Article
  14. Article
  15. Review
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 1 institution in 1 country.

Rita RosenthalDepartment of Gastroenterology, Rheumatology and Infectious Diseases, Section Nutritional Medicine/Clinical Physiology, Charité, Campus Benjamin Franklin, 12200, Berlin, Germany. rita.rosenthal@charite.de.
Julia LuettigDepartment of Gastroenterology, Rheumatology and Infectious Diseases, Section Nutritional Medicine/Clinical Physiology, Charité, Campus Benjamin Franklin, 12200, Berlin, Germany.
Nina A HeringDepartment of General, Visceral and Vascular Surgery, Charité, Campus Benjamin Franklin, Berlin, Germany.
Susanne M KrugDepartment of Gastroenterology, Rheumatology and Infectious Diseases, Section Nutritional Medicine/Clinical Physiology, Charité, Campus Benjamin Franklin, 12200, Berlin, Germany.
Uwe AlbrechtMediconomics GmbH, Hannover, Germany.
Michael FrommDepartment of Gastroenterology, Rheumatology and Infectious Diseases, Section Nutritional Medicine/Clinical Physiology, Charité, Campus Benjamin Franklin, 12200, Berlin, Germany.
Jörg-Dieter SchulzkeDepartment of Gastroenterology, Rheumatology and Infectious Diseases, Section Nutritional Medicine/Clinical Physiology, Charité, Campus Benjamin Franklin, 12200, Berlin, Germany.
Charité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeMyrrh, the oleo-gum resin of Commiphora molmol, is well known for its anti-inflammatory properties. In different animal models, it protected against DSS-, TNBS- and oxazolone-induced colitis. To date, no information concerning the effect of myrrh on barrier properties are available. Thus, this study investigates the effect of myrrh on paracellular barrier function in the absence or presence of the pro-inflammatory cytokine TNFα.

methodsMonolayers of human colon cell lines HT-29/B6 and Caco-2 were incubated with myrrh under control conditions or after challenge with the pro-inflammatory cytokine TNFα. Barrier function was analysed by electrophysiological and permeability measurements, Western blotting, immunostaining in combination with confocal microscopy, and freeze-fracture electron microscopy.

resultsIn Caco-2 cells, myrrh induced an increase in transepithelial resistance (TER) which was associated with downregulation of the channel-forming tight junction (TJ) protein claudin-2 via inhibition of the PI3 kinase signalling pathway. In HT-29/B6 cells, myrrh had no effect on barrier properties under basic conditions, but protected against barrier damage induced by TNFα, as indicated by a decrease in TER and an increase in fluorescein permeability. The TNFα effect was associated with a redistribution of the sealing TJ protein claudin-1, an increase in the expression of claudin-2 and a change in TJ ultrastructure. Most importantly, all TNFα effects were inhibited by myrrh. The effect of myrrh on claudin-2 expression in this cell line was mediated via inhibition of the STAT6 pathway.

conclusionsThis study shows for the first time that myrrh exerts barrier-stabilising and TNFα-antagonising effects in human intestinal epithelial cell models via inhibition of PI3K and STAT6 signalling. This suggests therapeutic application of myrrh in intestinal diseases associated with barrier defects and inflammation.

Indexed as

Caco-2 CellsChamomileCharcoalCoffeeCommiphoraEnterocytesHT29 CellsHumansModels, BiologicalProtective AgentsProtein TransportResins, PlantSignal TransductionTight Junction ProteinsTight JunctionsTumor Necrosis Factor-alphaCharcoalCoffeemyrrh resinProtective AgentsResins, PlantTight Junction ProteinsTumor Necrosis Factor-alphaChannel-forming claudin-2MyrrhParacellular permeabilitySealing claudin-1Tight junctionTNFα

Identifiers

PMID27981377
OpenAlexW2563819628

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.