Caffeic acid phenethyl ester protects against oxidative stress and dampens inflammation via heme oxygenase 1 / 国际口腔科学杂志·英文版
International Journal of Oral Science
; (4): 6-6, 2019.
Article
en En
| WPRIM
| ID: wpr-772276
Biblioteca responsable:
WPRO
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.
Texto completo:
1
Índice:
WPRIM
Asunto principal:
Farmacología
/
Alcohol Feniletílico
/
Ácidos Cafeicos
/
FN-kappa B
/
Estrés Oxidativo
/
Quimioterapia
/
Hemo-Oxigenasa 1
/
Genética
/
Inflamación
/
Metabolismo
Tipo de estudio:
Prognostic_studies
Límite:
Animals
/
Humans
Idioma:
En
Revista:
International Journal of Oral Science
Año:
2019
Tipo del documento:
Article