HOST NUCLEAR FACTOR ERYTHROID 2-RELATED FACTOR-2 DEFENSE SYSTEM DETERMINES THE OUTCOME OF DEXTRAN SULFATE SODIUM-INDUCED COLITIS IN MICE
DC Field | Value | Language |
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dc.contributor.author | Lee, J. S. | - |
dc.contributor.author | An, J. M. | - |
dc.contributor.author | Kang, E. A. | - |
dc.contributor.author | Han, Y. M. | - |
dc.contributor.author | Kim, Y. S. | - |
dc.contributor.author | Lee, H. J. | - |
dc.contributor.author | Kim, K-J | - |
dc.contributor.author | Surh, Y. J. | - |
dc.contributor.author | Hahm, K-B | - |
dc.date.available | 2020-02-27T09:41:16Z | - |
dc.date.created | 2020-02-06 | - |
dc.date.issued | 2018-10 | - |
dc.identifier.issn | 0867-5910 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/3307 | - |
dc.description.abstract | Administration of dextran sulfate sodium (DSS) in drinking water led to significant bout of colitis simulating ulcerative colitis of human. However, colitis usually developed 5 - 7 days after DSS administration. Therefore, we hypothesized host defense system might protect colitis up to 5 days of DSS administration. 2.5% DSS-induced colitis were administered to C57BL/6 mice and sequential measurements of pathology, cyclooxygenase-2 (COX-2), nuclear factor-kappa B (NF-kappa B), heme oxygenase-1 (HO-1), NADPH quinone oxidoreductase-1 (NQO1), gamma-glutamylcysteine synthetase (gamma-GCS), nuclear factor erythroid 2-related factor-2 (Nrf2), and keap1 were done at 2, 6, 12, 24, 48, 96, 120, and 168 hour of DSS administration, respectively. DSS-induced colitis was repeated in either COX-2(-/-) or Nrf2(-/-) mice. On serial pathological analysis, significant colitis was noted after 120 h of DSS administration, during which both activations of COX-2/NF-kappa B and HO-1/Nrf2 were noted. Nrf2 activations after keap1 inactivation led to significant increases in HO-1 after 168 hours of DSS administration, when NF-kappa B nuclear translocation was noted. Significantly attenuated colitis was noted in DSS-challenged COX-2(-/-) mice, in which the levels of HO-1 were significantly decreased compared to DSS-challenged WT littermates (p < 0.01), while the levels of NQO1 were significantly increased. On DSS administration to Nrf2(-/-) mice, colitis was significantly aggravated (p < 0.01), in which the expressions of COX-2 as well as expressions of HO-1 and gamma-GCS were significantly increased (p < 0.01). Reciprocal activations of inflammatory and antioxidative defense signaling after DSS administration might be prerequisite to make intestinal homeostasis and host defense Nrf2 system can determine colitis. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | POLISH PHYSIOLOGICAL SOC | - |
dc.relation.isPartOf | JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY | - |
dc.subject | CHRONIC ULCERATIVE-COLITIS | - |
dc.subject | HEME OXYGENASE-1 | - |
dc.subject | OXIDATIVE STRESS | - |
dc.subject | CARBON-MONOXIDE | - |
dc.subject | MURINE MODEL | - |
dc.subject | NRF2 | - |
dc.subject | INFLAMMATION | - |
dc.subject | INDUCTION | - |
dc.subject | DYSPLASIA | - |
dc.subject | ENZYMES | - |
dc.title | HOST NUCLEAR FACTOR ERYTHROID 2-RELATED FACTOR-2 DEFENSE SYSTEM DETERMINES THE OUTCOME OF DEXTRAN SULFATE SODIUM-INDUCED COLITIS IN MICE | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000457073300010 | - |
dc.identifier.doi | 10.26402/jpp.2018.5.10 | - |
dc.identifier.bibliographicCitation | JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY, v.69, no.5, pp.755 - 767 | - |
dc.identifier.scopusid | 2-s2.0-85060515439 | - |
dc.citation.endPage | 767 | - |
dc.citation.startPage | 755 | - |
dc.citation.title | JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY | - |
dc.citation.volume | 69 | - |
dc.citation.number | 5 | - |
dc.contributor.affiliatedAuthor | Lee, H. J. | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | experimental | - |
dc.subject.keywordAuthor | colitis | - |
dc.subject.keywordAuthor | nuclear factor erythroid 2-related factor-2 | - |
dc.subject.keywordAuthor | heme oxygenase-1 | - |
dc.subject.keywordAuthor | cyclooxygenase-2 | - |
dc.subject.keywordAuthor | keap 1 | - |
dc.subject.keywordAuthor | host defense system | - |
dc.subject.keywordAuthor | intestinal permeability | - |
dc.subject.keywordPlus | CHRONIC ULCERATIVE-COLITIS | - |
dc.subject.keywordPlus | HEME OXYGENASE-1 | - |
dc.subject.keywordPlus | OXIDATIVE STRESS | - |
dc.subject.keywordPlus | CARBON-MONOXIDE | - |
dc.subject.keywordPlus | MURINE MODEL | - |
dc.subject.keywordPlus | NRF2 | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.subject.keywordPlus | INDUCTION | - |
dc.subject.keywordPlus | DYSPLASIA | - |
dc.subject.keywordPlus | ENZYMES | - |
dc.relation.journalResearchArea | Physiology | - |
dc.relation.journalWebOfScienceCategory | Physiology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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