Caffeic acid phenethyl ester protects against oxidative stress and dampens inflammation via heme oxygenase 1.
10.1038/s41368-018-0039-5
- Author:
Alexandra STÄHLI
1
;
Ceeneena Ubaidha MAHEEN
1
;
Franz Josef STRAUSS
1
;
Sigrun EICK
2
;
Anton SCULEAN
2
;
Reinhard GRUBER
3
Author Information
1. Department of Oral Biology, School of Dentistry, Medical University of Vienna, Sensengasse 2a, Vienna, Austria.
2. Department of Periodontology, School of Dental Medicine, University of Bern, Freiburgstrasse 7, Bern, Switzerland.
3. Department of Oral Biology, School of Dentistry, Medical University of Vienna, Sensengasse 2a, Vienna, Austria. reinhard.gruber@meduniwien.ac.at.
- Publication Type:Journal Article
- MeSH:
Animals;
Caffeic Acids;
pharmacology;
Heme Oxygenase-1;
genetics;
metabolism;
Humans;
Inflammation;
drug therapy;
Mice;
NF-kappa B;
antagonists & inhibitors;
genetics;
metabolism;
Oxidative Stress;
drug effects;
Phenylethyl Alcohol;
analogs & derivatives;
pharmacology
- From:
International Journal of Oral Science
2019;11(1):6-6
- CountryChina
- Language:English
-
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.
