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Suppression of NF-kappaB activation and cytokine production by N-acetylcysteine in pancreatic acinar cells.

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dc.contributor.author김경환-
dc.date.accessioned2019-11-11T05:08:03Z-
dc.date.available2019-11-11T05:08:03Z-
dc.date.issued2000-
dc.identifier.issn0891-5849-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/171638-
dc.description.abstractReactive oxygen species (ROS), generated by infiltrating neutrophils, are considered as an important regulator in the pathogenesis and development of pancreatitis. A hallmark of the inflammatory response is the induction of cytokine gene expression, which may be regulated by oxidant-sensitive transcription factor, nuclear factor-kappaB (NF-kappaB). Present study aims to investigate whether neutrophils primed by 4beta-phorbol 12beta-myristate 13alpha-acetate (PMA) affect the productions of H(2)O(2) and lipid peroxide (LPO), NF-kappaB activation and cytokine production in pancreatic acinar cells, and whether these alterations were inhibited by N-acetylcysteine (NAC) and superoxide dismutase (SOD). Neutrophils generated ROS by stimulation with PMA, which was inhibited by NAC and SOD. In acinar cells, PMA-primed neutrophils increased the productions of H(2)O(2), LPO, and cytokines both time and dose dependently. PMA-primed neutrophils resulted in the activation of two species of NF-kappaB dimers (a p50/p65 heterodimer and a p50 homodimer) in acinar cells. Both NAC and SOD inhibited neutrophil-induced, oxidant-mediated alterations in acinar cells. In conclusion, ROS, generated by neutrophils, activates NF-kappaB, resulting in upregulation of inflammatory cytokines in acinar cells. Antioxidants such as NAC might be useful antiinflammatory agents by inhibiting oxidant-mediated activation of NF-kappaB and decreasing cytokine production.-
dc.description.statementOfResponsibilityrestriction-
dc.languageEnglish-
dc.publisherElsevier Science-
dc.relation.isPartOfFree Radical Biology and Medicine-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.subject.MESHAcetylcysteine/pharmacology*-
dc.subject.MESHAnimals-
dc.subject.MESHAntioxidants/pharmacology*-
dc.subject.MESHCells, Cultured-
dc.subject.MESHCytokines/analysis-
dc.subject.MESHCytokines/genetics*-
dc.subject.MESHGene Expression Regulation/drug effects-
dc.subject.MESHGene Expression Regulation/immunology*-
dc.subject.MESHHydrogen Peroxide/metabolism-
dc.subject.MESHKinetics-
dc.subject.MESHLipid Peroxidation/drug effects*-
dc.subject.MESHMale-
dc.subject.MESHNF-kappa B/antagonists & inhibitors*-
dc.subject.MESHPancreas/drug effects-
dc.subject.MESHPancreas/immunology-
dc.subject.MESHPancreas/physiology*-
dc.subject.MESHRNA, Messenger/genetics-
dc.subject.MESHRats-
dc.subject.MESHRats, Sprague-Dawley-
dc.subject.MESHSuperoxide Dismutase/metabolism-
dc.subject.MESHTetradecanoylphorbol Acetate/pharmacology-
dc.subject.MESHTime Factors-
dc.subject.MESHTranscription, Genetic/drug effects-
dc.titleSuppression of NF-kappaB activation and cytokine production by N-acetylcysteine in pancreatic acinar cells.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pharmacology (약리학교실)-
dc.contributor.googleauthorHyeyoung Kim-
dc.contributor.googleauthorJeong Yeon Seo-
dc.contributor.googleauthorKwan Ho Roh-
dc.contributor.googleauthorJoo Weon Lim-
dc.contributor.googleauthorKyung Hwan Kim-
dc.identifier.doi10.1016/S0891-5849(00)00368-3-
dc.contributor.localIdA00311-
dc.relation.journalcodeJ00906-
dc.identifier.eissn1873-4596-
dc.identifier.pmid11033420-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0891584900003683-
dc.subject.keywordReactive oxygen species-
dc.subject.keywordNF-κB-
dc.subject.keywordCytokine-
dc.subject.keywordPancreatic acinar cells-
dc.subject.keywordNeutrophils-
dc.subject.keywordN-acetylcysteine-
dc.subject.keywordFree radicals-
dc.contributor.alternativeNameKim, Kyung Hwan-
dc.contributor.affiliatedAuthor김경환-
dc.citation.volume29-
dc.citation.number7-
dc.citation.startPage674-
dc.citation.endPage683-
dc.identifier.bibliographicCitationFree Radical Biology and Medicine, Vol.29(7) : 674-683, 2000-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers

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