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Anti-Inflammatory Mechanism of Polyunsaturated Fatty Acids in Helicobacter pylori-Infected Gastric Epithelial Cells

Authors
Lee, Sun EunLim, Joo WeonKim, Jung MoggKim, Hyeyoung
Issue Date
Jun-2014
Publisher
HINDAWI LTD
Citation
MEDIATORS OF INFLAMMATION, v.2014, no.6, pp.1 - 12
Indexed
SCIE
SCOPUS
Journal Title
MEDIATORS OF INFLAMMATION
Volume
2014
Number
6
Start Page
1
End Page
12
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/159815
DOI
10.1155/2014/128919
ISSN
0962-9351
Abstract
Helicobacter pylori is an important risk factor for gastric inflammation, which is mediated by multiple signaling pathways. The aim of this study was to investigate the effects of polyunsaturated fatty acids (PUFAs), such as linoleic acid (LA), alpha-linolenic acid (ALA), and docosahexaenoic acid (DHA), on the expression of the proinflammatory chemokine interleukin-8 (IL-8) in H. pylori-infected gastric epithelial AGS cells. To investigate whether PUFAs modulate H. pylori-induced inflammatory signaling, we determined the activation of epidermal growth factor receptor (EGFR), protein kinase C-delta (PKC delta), mitogen-activated protein kinases (MAPKs), nuclear factor-kappa B (NF-kappa B), and activator protein-1 (AP-1) as well as IL-8 expression in H. pylori-infected gastric epithelial cells that had been treated with or without PUFAs. We found that PUFAs inhibited IL-8 mRNA and protein expression in H. pylori-infected cells. omega-3 fatty acids (ALA, and DHA) suppressed the activation of EGFR, PKC delta, MAPK, NF-kappa B, and AP-1 in these infected cells. LA did not prevent EGFR transactivation and exhibited a less potent inhibitory effect on IL-8 expression than did ALA and DHA. In conclusion, PUFAs may be beneficial for prevention of H. pylori-associated gastric inflammation by inhibiting proinflammatory IL-8 expression.
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