Evidence map›Paper›PMID 30783082›Full record

ArticleInternational journal of oral science2019

Caffeic acid phenethyl ester protects against oxidative stress and dampens inflammation via heme oxygenase 1.

Alexandra Stähli, Ceeneena Ubaidha Maheen, Franz Josef Strauss, Sigrun Eick, Anton Sculean, Reinhard Gruber

Open access · goldAbstract read
In one paragraph

Article in International journal of oral science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 72 citations in OpenAlex.

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  15. Neuroprotective Effect ofCurrent pharmaceutical biotechnology · 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

6 authors at 3 institutions in 3 countries.

Alexandra StähliDepartment of Oral Biology, School of Dentistry, Medical University of Vienna, Sensengasse 2a, Vienna, Austria.ORCID http://orcid.org/0000-0002-5631-3300
Ceeneena Ubaidha MaheenDepartment of Oral Biology, School of Dentistry, Medical University of Vienna, Sensengasse 2a, Vienna, Austria.
Franz Josef StraussDepartment of Oral Biology, School of Dentistry, Medical University of Vienna, Sensengasse 2a, Vienna, Austria.ORCID http://orcid.org/0000-0002-5832-7327
Sigrun EickDepartment of Periodontology, School of Dental Medicine, University of Bern, Freiburgstrasse 7, Bern, Switzerland.ORCID http://orcid.org/0000-0002-4619-2461
Anton SculeanDepartment of Periodontology, School of Dental Medicine, University of Bern, Freiburgstrasse 7, Bern, Switzerland.
Reinhard GruberDepartment of Oral Biology, School of Dentistry, Medical University of Vienna, Sensengasse 2a, Vienna, Austria. reinhard.gruber@meduniwien.ac.at.ORCID http://orcid.org/0000-0001-5400-9009
University of Bern · CHMedical University of Vienna · ATUniversity of Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Periodontal disease is associated with chronic oxidative stress and inflammation. Caffeic acid phenethyl ester (CAPE), which is a potent inducer of heme oxygenase 1 (HO1), is a central active component of propolis, and the application of propolis improves periodontal status in diabetic patients. Here, primary murine macrophages were exposed to CAPE. Target gene expression was assessed by whole-genome microarray, RT-PCR and Western blotting. The antioxidative and anti-inflammatory activities of CAPE were examined by exposure of the cells to hydrogen peroxide, saliva and periodontal pathogens. The involvement of HO1 was investigated with the HO1 inhibitor tin protoporphyrin (SnPP) and knockout mice for Nrf2, which is a transcription factor for detoxifying enzymes. CAPE increased HO1 and other heat shock proteins in murine macrophages. A p38 MAPK inhibitor and Nrf2 knockout attenuated CAPE-induced HO1 expression in macrophages. CAPE exerted strong antioxidative activity. Additionally, CAPE reduced the inflammatory response to saliva and periodontal pathogens. Blocking HO1 decreased the antioxidative activity and attenuated the anti-inflammatory activity of CAPE. In conclusion, CAPE exerted its antioxidative effects through the Nrf2-mediated HO1 pathway and its anti-inflammatory effects through NF-κB inhibition. However, preclinical models evaluating the use of CAPE in periodontal inflammation are necessary in future studies.

Indexed as

Heme Oxygenase-1Phenylethyl AlcoholAnimalsCaffeic AcidsHumansInflammationMiceNF-kappa BOxidative Stresscaffeic acid phenethyl esterCaffeic AcidsHeme Oxygenase-1NF-kappa BPhenylethyl Alcohol

Identifiers

PMID30783082
PMCPMC6381107
OpenAlexW2907739570

What OpenQuestion holds

Textmetadata
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.