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Suppression of IL-1β expression by the Jak 2 inhibitor AG490 in cerulein-stimulated pancreatic acinar cells

DC FieldValueLanguage
dc.contributor.author김경환-
dc.contributor.author김혜영-
dc.date.accessioned2015-06-10T13:03:49Z-
dc.date.available2015-06-10T13:03:49Z-
dc.date.issued2006-
dc.identifier.issn0006-2952-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/110939-
dc.description.abstractCerulein pancreatitis is similar to human edematous pancreatitis with dysregulation of the digestive enzyme production and cytoplasmic vacuolization, the death of acinar cells, edema formation, and an infiltration of inflammatory cells into the pancreas. Cytokines are up-regulated in pancreatic acinar cells stimulated with cerulein. In various cells and tissues, Janus kinase (Jak)/signal transducer and activator of transcription (Stat) pathway mediates inflammatory process. In the present study, we investigated whether the activation of Jak/Stat signaling mediates IL-1β expression in pancreatic acinar AR42J cells stimulated with cerulein in vitro as well as the rats with cerulein pancreatitis in vivo using AG490, the Jak2 inhibitor. Activation of Jak2 and Stat3 were monitored by Western blot analysis for phosphorylated Jak2 and phosphorylated Stat3. mRNA expression and protein level of IL-1β were determined by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbant assay (ELISA). Histological examination of pancreatic tissues were performed and serum IL-1β levels of the rats were determined by ELISA. As a result, cerulein induced the activation of Jak2 and Stat3 as well as IL-1β expression, which was inhibited by the treatment of AG490 in AR42J cells. In cerulein pancreatitis of the rats, edematous and inflammatory changes of the pancreas and increased serum levels of IL-1β were suppressed by AG490 treatment. In conclusion, Jak2/Stat3 pathway may be the underlying mechanism in the pathogenesis of pancreatitis by inducing cytokines such as IL-1β.-
dc.description.statementOfResponsibilityopen-
dc.format.extent1555~1562-
dc.relation.isPartOfBIOCHEMICAL PHARMACOLOGY-
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.MESHCells, Cultured-
dc.subject.MESHCeruletide/pharmacology*-
dc.subject.MESHDisease Models, Animal-
dc.subject.MESHDrug Therapy, Combination-
dc.subject.MESHEnzyme Inhibitors/pharmacology*-
dc.subject.MESHGene Expression/drug effects-
dc.subject.MESHInterleukin-1beta/antagonists & inhibitors*-
dc.subject.MESHInterleukin-1beta/genetics-
dc.subject.MESHInterleukin-1beta/metabolism-
dc.subject.MESHJanus Kinase 2/antagonists & inhibitors-
dc.subject.MESHJanus Kinase 2/biosynthesis-
dc.subject.MESHMale-
dc.subject.MESHPancreas/drug effects*-
dc.subject.MESHPancreas/metabolism-
dc.subject.MESHPancreas/pathology-
dc.subject.MESHPancreatitis/chemically induced-
dc.subject.MESHPancreatitis/metabolism*-
dc.subject.MESHPancreatitis/pathology-
dc.subject.MESHPhosphorylation-
dc.subject.MESHRNA, Messenger/metabolism-
dc.subject.MESHRats-
dc.subject.MESHRats, Sprague-Dawley-
dc.subject.MESHSTAT3 Transcription Factor/biosynthesis-
dc.subject.MESHTyrphostins/pharmacology*-
dc.titleSuppression of IL-1β expression by the Jak 2 inhibitor AG490 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.identifier.doi10.1016/j.bcp.2006.07.008-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00311-
dc.contributor.localIdA01175-
dc.relation.journalcodeJ00283-
dc.identifier.eissn1873-2968-
dc.identifier.pmid16934228-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0006295206004242-
dc.subject.keywordCeruleinIL-1β-
dc.subject.keywordJak/Stat-
dc.subject.keywordAG490-
dc.subject.keywordPancreatic acinar cells-
dc.contributor.alternativeNameKim, Kyung Hwan-
dc.contributor.alternativeNameKim, Hye Young-
dc.contributor.affiliatedAuthorKim, Kyung Hwan-
dc.contributor.affiliatedAuthorKim, Hye Young-
dc.rights.accessRightsnot free-
dc.citation.volume72-
dc.citation.number11-
dc.citation.startPage1555-
dc.citation.endPage1562-
dc.identifier.bibliographicCitationBIOCHEMICAL PHARMACOLOGY, Vol.72(11) : 1555-1562, 2006-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers

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