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Please use this identifier to cite or link to this item: http://hdl.handle.net/2262/33813

Title: Caffeic acid phenethyl ester modulates Helicobacter pylori-induced nuclear factor-kappa B and activator protein-1 expression in gastric epithelial cells
Author: KELLEHER, DERMOT P
SABRA, KAMAL
WINDLE, HENRY
Sponsor: Higher Education Authority
Author's Homepage: http://people.tcd.ie/kellehdp
Keywords: Clinical Medicine
Issue Date: 2005
Publisher: Nature
Citation: Mohamed MM Abdel-Latif, Henry J Windle, Basma S El Homasany, Kamal Sabra, Dermot Kelleher, ‘Caffeic acid phenethyl ester modulates Helicobacter pylori-induced nuclear factor-kappa B and activator protein-1 expression in gastric epithelial cells’ in British Journal of Pharmacology, 146, (8), 2005, pp 1139 - 1147
Series/Report no.: British Journal of Pharmacology
146
8
Abstract: Caffeic acid phenethyl ester (CAPE), an active component of propolis from honeybee hives (honeybee resin), has anti-inflammatory, anti-carcinogenic and anti-bacterial properties. This study was designed to investigate the anti-inflammatory effects of CAPE on Helicobacter pylori-induced NF-kappaB and AP-1 in the gastric epithelial cell line AGS. Electrophoretic mobility shift assay was used to measure NF-kappaB- and AP-1-DNA binding activity. Western blotting was used to detect IkappaB-alpha and COX-2 expression in AGS cells cocultured with H. pylori. The antiproliferative effect of CAPE was measured by MTT assay. Our results showed that caffeic phenethyl ester inhibits H. pylori-induced NF-kappaB and AP-1 DNA-binding activity in a dose (0.1-25 microg ml(-1) approximately 0.35-88 microM) and time- (15-240 min) dependent manner in AGS cells. Maximum inhibition by CAPE was observed at concentrations of 25 microg ml(-1) ( approximately 88 microM) CAPE prevented H. pylori- and cytokine-induced degradation of IkappaB-alpha protein. Pretreatment of AGS cells with CAPE also blocked cytokine- and mitogen-induced NF-kappaB and AP-1 expression. Furthermore, CAPE suppressed H. pylori-induced cell proliferation and production of the cytokines TNF-alpha and IL-8. In addition, CAPE blocked H. pylori-induced COX-2 expression. The inhibition of such transcription by CAPE could result in suppression of many genes during H. pylori-induced inflammation, and also provide new insights into the anti-cancer and anti-inflammatory properties of CAPE.
Description: PUBLISHED
URI: http://dx.doi.org/0.1038/sj.bjp.0706421.
http://hdl.handle.net/2262/33813
Appears in Collections:Administrative Staff Authors (Scholarly Publications)

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