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The phenyl-thiophenyl propenone RK-I-123 reduces the levels of reactive oxygen species and suppresses the activation of NF-kappa B and AP-1 and IL-8 expression in Helicobacter pylori-infected gastric epithelial AGS cells

Authors
Jang, Sung HeeCho, SoonokLee, Eung-SeokKim, Jung MoggKim, Hyeyoung
Issue Date
Jul-2013
Publisher
Birkhauser Verlag
Keywords
Helicobacter pylori; RK-I-123; IL-8; NF-kappa B; Gastric epithelial cells
Citation
Inflammation Research, v.62, no.7, pp 689 - 696
Pages
8
Indexed
SCI
SCIE
SCOPUS
Journal Title
Inflammation Research
Volume
62
Number
7
Start Page
689
End Page
696
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/162401
DOI
10.1007/s00011-013-0621-4
ISSN
1023-3830
1420-908X
Abstract
To investigate whether the phenyl-thiophenyl propenone RK-I-123 suppresses interleukin-8 (IL-8) expression and activation of mitogen-activated protein kinases (MAPKs) and transcription factors (nuclear factor-kappa B [NF-kappa B] and activator protein-1 [AP-1]) by reducing reactive oxygen species (ROS) levels in Helicobacter pylori-infected gastric epithelial cells. Helicobacter pylori in Korean isolates, human gastric epithelial AGS cells. AGS cells pretreated with or without RK-I-123 were cultured in the presence of H. pylori at a bacterium/cell ratio of 300:1. Reactive oxygen species and IL-8 levels were determined by dichlorofluorescein fluorescence and enzyme-linked immunosorbent assay. The IL-8 mRNA expression was analyzed by the real-time reverse transcription-polymerase chain reaction (RT-PCR). The MAPK and I kappa B alpha levels were determined by western blotting. The activation of NF-kappa B and AP-1 was determined by the electrophoretic mobility shift assay. Helicobacter pylori induced an increase in ROS and IL-8 expression and activation of MAPKs and transcription factors (NF-kappa B and AP-1) together with the degradation of I kappa B alpha in AGS cells, all of which were inhibited by RK-I-123. The RK-I-123 suppressed the H. pylori-induced IL-8 expression and activation of MAPKs, NF-kappa B, and AP-1 by reducing ROS levels in AGS cells. The RK-I-123 may be a potential candidate for the treatment of H. pylori-induced gastric inflammation.
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