Cited 27 times in

Diphenyleneiodonium suppresses apoptosis in cerulein-stimulated pancreatic acinar cells

DC Field Value Language
dc.contributor.author김경환-
dc.contributor.author김동구-
dc.date.accessioned2014-12-21T16:40:23Z-
dc.date.available2014-12-21T16:40:23Z-
dc.date.issued2007-
dc.identifier.issn1357-2725-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/96132-
dc.description.abstractNADPH oxidase has been considered a major source of reactive oxygen species in phagocytic and non-phagocytic cells. Apoptosis linked to oxidative stress has been implicated in pancreatitis. Recently, we demonstrated that NADPH oxidase subunits Nox1, p27phox, p47phox, and p67phox are constitutively expressed in pancreatic acinar cells, which are activated by cerulein, a cholecystokinin analogue. Cerulein induces an acute and edematous form of pancreatitis. We investigated whether inhibition of NADPH oxidase by diphenyleneiodonium suppresses the production of reactive oxygen species and apoptosis by determining viable cell numbers, DNA fragmentation, TUNEL staining, caspase-3 activity, and the expression of apoptosis-inducing factor in pancreatic acinar AR42J cells stimulated with cerulein. Inhibition on NADPH oxidase by diphenyleneiodonium was assessed by the alterations in NADPH oxidase activity and translocation of the cytosolic subunits p67phox and p47phox to the membrane. Intracellular Ca2+ level was monitored to investigate the relationship between NADPH oxidase and Ca2+ in cells stimulated with cerulein. As a result, cerulein induced the activation of NADPH, increased production of reactive oxygen species, and apoptotic indices determined by the expression of apoptosis-inducing factor, caspase-3 activation, TUNEL staining, DNA fragmentation, and cell viability. Treatment with DPI inhibited cerulein-induced activation of NADPH oxidase, the production of reactive oxygen species, and apoptosis, but not the increase of intracellular Ca2+ levels in pancreatic acinar cells. These results demonstrate that the cerulein-induced increase in intracellular Ca2+ level may be an upstream event of NADPH oxidase activation. Diphenyleneiodonium, an NADPH oxidase inhibitor, inhibits the expression of apoptosis-inducing factor and caspase-3 activation, and thus apoptosis in pancreatic acinar cells.-
dc.description.statementOfResponsibilityopen-
dc.format.extent2063~2075-
dc.relation.isPartOfINTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHApoptosis/drug effects*-
dc.subject.MESHApoptosis Inducing Factor/genetics-
dc.subject.MESHApoptosis Inducing Factor/metabolism-
dc.subject.MESHCalcium/metabolism-
dc.subject.MESHCaspase 3/metabolism-
dc.subject.MESHCell Line-
dc.subject.MESHCell Survival/drug effects-
dc.subject.MESHCeruletide/pharmacology*-
dc.subject.MESHDNA Fragmentation/drug effects-
dc.subject.MESHEnzyme Activation/drug effects-
dc.subject.MESHGene Expression Regulation/drug effects-
dc.subject.MESHGlutathione/pharmacology-
dc.subject.MESHIn Situ Nick-End Labeling-
dc.subject.MESHL-Lactate Dehydrogenase/metabolism-
dc.subject.MESHNADPH Oxidases/metabolism-
dc.subject.MESHOnium Compounds/pharmacology*-
dc.subject.MESHPancreas, Exocrine/cytology*-
dc.subject.MESHPancreas, Exocrine/drug effects*-
dc.subject.MESHPancreas, Exocrine/enzymology-
dc.subject.MESHPancreas, Exocrine/metabolism-
dc.subject.MESHRats-
dc.subject.MESHReactive Oxygen Species/metabolism-
dc.subject.MESHSuperoxide Dismutase/pharmacology-
dc.titleDiphenyleneiodonium suppresses apoptosis in cerulein-stimulated pancreatic acinar cells-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pharmacology (약리학)-
dc.contributor.googleauthorJi Hoon Yu-
dc.contributor.googleauthorKyung Hwan Kim-
dc.contributor.googleauthorHyeyoung Kim-
dc.contributor.googleauthorDong Goo Kim-
dc.identifier.doi10.1016/j.biocel.2007.05.021-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00311-
dc.contributor.localIdA00396-
dc.relation.journalcodeJ01089-
dc.identifier.eissn1878-5875-
dc.identifier.pmid17625947-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S135727250700177X-
dc.contributor.alternativeNameKim, Kyung Hwan-
dc.contributor.alternativeNameKim, Dong Goo-
dc.contributor.affiliatedAuthorKim, Kyung Hwan-
dc.contributor.affiliatedAuthorKim, Dong Goo-
dc.rights.accessRightsnot free-
dc.citation.volume39-
dc.citation.number11-
dc.citation.startPage2063-
dc.citation.endPage2075-
dc.identifier.bibliographicCitationINTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, Vol.39(11) : 2063-2075, 2007-
dc.identifier.rimsid35451-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers

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