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Supplementation with Angelica keiskei inhibits expression of inflammatory mediators in the gastric mucosa of Helicobacter pylori-infected mice

Authors
 Aryoung Kim  ;  Joo Weon Lim  ;  Hoguen Kim  ;  Hyeyoung Kim 
Citation
 NUTRITION RESEARCH, Vol.36(5) : 488-497, 2016 
Journal Title
 NUTRITION RESEARCH 
ISSN
 0271-5317 
Issue Date
2016
MeSH
Angelica/chemistry* ; Animals ; Anti-Inflammatory Agents ; Antioxidants ; DNA/metabolism ; Diet ; Gastric Mucosa/chemistry* ; Gastric Mucosa/drug effects ; Gastric Mucosa/microbiology ; Helicobacter Infections/prevention & control* ; Helicobacter pylori*/genetics ; Lipid Peroxides/analysis ; Mice ; Mice, Inbred C57BL ; NF-KappaB Inhibitor alpha/analysis ; NF-kappa B/antagonists & inhibitors ; NF-kappa B/drug effects ; NF-kappa B/metabolism ; Peroxidase/metabolism ; Phytotherapy ; Plant Extracts/administration & dosage* ; RNA, Bacterial/analysis ; RNA, Ribosomal, 16S/analysis
Keywords
Angelica keiskei ; Gastric mucosa ; Helicobacter pylori ; Inflammatory mediators ; Mice
Abstract
Oxidative stress is involved in the pathogenesis of Helicobacter pylori-associated gastric ulceration and carcinogenesis. The oxidant-sensitive transcription factor, nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB), regulates expression of inflammatory mediators such as interferon γ (IFN-γ), cyclooxygenase 2 (COX-2), and inducible nitric oxide synthase (iNOS). These inflammatory mediators increased in gastric mucosal tissues from patients infected with H pylori. Angelica keiskei (AK), a green leafy vegetable, is rich in carotenoids and flavonoids and shows antioxidant and anti-inflammatory activities. Therefore, we hypothesized that AK may protect the gastric mucosa of H pylori-infected mice against inflammation. We determined lipid peroxide abundance, myeloperoxidase activity, expression levels of inflammatory mediators (IFN-γ, COX-2, and iNOS), NF-κB-DNA binding activity, and histologic changes in gastric mucosal tissues. The antioxidant N-acetylcysteine served as the positive control treatment. Supplementation with AK suppressed increases in lipid peroxide abundance, myeloperoxidase activity, induction of inflammatory mediators (IFN-γ, COX-2, and iNOS), activation of NF-κB, and degradation of nuclear factor of κ light polypeptide gene enhancer in B-cells inhibitor α in gastric mucosal tissue from H pylori-infected mice. Inhibition of H pylori-induced alterations by AK was similar to that by N-acetylcysteine. Taken together, these results suggest that supplementation with AK may prevent H pylori-induced gastric inflammation by inhibiting NF-κB-mediated induction of inflammatory mediators in the gastric mucosa of patients infected with H pylori.
Full Text
http://www.sciencedirect.com/science/article/pii/S0271531716000038
DOI
10.1016/j.nutres.2015.12.017
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
Yonsei Authors
Kim, Hogeun(김호근)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/146508
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