| Project/Area Number |
14570493
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
NAITO Yuji Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Assistant Professor, 医学研究科, 助手 (00305575)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIKAWA Toshikazu Kyoto Prefectural University of Medicine, Graduate School of Medical Science, Professor, 医学研究科, 教授 (90158410)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2003: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2002: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | ulcerative colitis / experimental model of colitis / transcriptional factor / molecular target therapy / inflammatory cytokines / spin trapping agent / pioglitazone / gene expression regulation / 炎症性腸疾患 / NF-κB / PPAR / 核内受容体 |
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| Research Abstract |
Using a model of dextran sulfate sodium (DSS)-induced colitis in mice, we have demonstrated the following findings; 1)the activity of NF-kB determined by EMSA assay was enhanced in the course of colitis; 2)the gene expression of NE-kB-related genes such as inducible NO synthase and pro-inflammatory cytokines was upregulated related with NF-kB activation; 3)the activation of NF-kB correlated with the development intestinal inflammation and clinical index of colitis; 4)the inhibitors of NF-kB activation (spin trappin agent PBN, PPAR-g ligand pioglitazone, antioxidant vitamin E derivative) demonstrate the inhibition of DSS-induced colitis ; and 5)NF-kB activation and intestinal inflammation was enhanced in tumor necrosis factor-deficient mice. These results indicate that NF-kB-dependent gene transcription plays a critical role in the pathogenesis of DSS-induced colitis in mice.
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