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Transcriptional regulation by thiol compounds in Helicobacter pylori-induced IL-8 production in human gastric epithelial cells

DC FieldValueLanguage
dc.contributor.author김경환-
dc.date.accessioned2016-05-16T10:54:48Z-
dc.date.available2016-05-16T10:54:48Z-
dc.date.issued2002-
dc.identifier.issn0077-8923-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/143389-
dc.description.abstractReactive oxygen species (ROS) have been counted among the potential toxic factors involving Helicobacter pylori (H. pylori)-induced gastric injury. Transcription nuclear factor-κB (NF-κB) is activated by ROS and regulates inflammatory gene expression. Thiol compounds, such as glutathione and N-acetylcysteine, scavenge hydrogen peroxide and are reported to prevent oxidative damage in various cells. The present study aims to investigate whether thiol compounds could affect H. pylori-induced IL-8 production by regulating transcription factor NF-κB in human gastric epithelial AGS cells. AGS cells were incubated with H. pylori (NCTC 11637) at a ratio of 1:100 in the presence or absence of thiol compounds. ROS generation was determined by confocal microscopy using ROS-sensitive dichlorofluorescein diacetate dye. Levels of hydrogen peroxide and IL-8 in the medium and DNA binding activity of NF-κB were determined by enzyme-linked immunosorbent assay, colorimetric assay, and electrophoretic mobility shift assay. Results indicated both thiol compounds inhibited H. pylori-induced hydrogen peroxide production, in accordance with their inhibition on NF-κB activation and IL-8 production induced by H. pylori in AGS cells. In conclusion, ROS may be a signaling molecule triggering NF-κB activation and the expression of inflammatory genes such as IL-8.-
dc.description.statementOfResponsibilityopen-
dc.format.extent541~545-
dc.relation.isPartOfANNALS OF THE NEW YORK ACADEMY OF SCIENCES-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleTranscriptional regulation by thiol compounds in Helicobacter pylori-induced IL-8 production in human gastric epithelial cells-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pharmacology (약리학)-
dc.contributor.googleauthorJeong Yeon Seo-
dc.contributor.googleauthorHyeyoung Kim-
dc.contributor.googleauthorKyung Hwan Kim-
dc.identifier.doi10.1111/j.1749-6632.2002.tb04697.x-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00311-
dc.relation.journalcodeJ00181-
dc.identifier.eissn1749-6632-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1111/j.1749-6632.2002.tb04697.x/abstract-
dc.contributor.alternativeNameKim, Kyung Hwan-
dc.contributor.affiliatedAuthorKim, Kyung Hwan-
dc.rights.accessRightsnot free-
dc.citation.volume973-
dc.citation.startPage541-
dc.citation.endPage545-
dc.identifier.bibliographicCitationANNALS OF THE NEW YORK ACADEMY OF SCIENCES, Vol.973 : 541-545, 2002-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers

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