| Project/Area Number |
06670220
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Experimental pathology
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| Research Institution | Gifu University |
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Principal Investigator |
MORI Hideki Gifu University School of Medicine Professor, 医学部, 教授 (70021433)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIMI Naoki Gifu University School of Medicine Senior Instructor, 医学部, 講師 (30166996)
TANAKA Takuji Gifu University School of Medicine Associate Professor, 医学部, 助教授 (40126743)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1995: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1994: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Cytokines / TNF-a / IL-la / MAM acetate / Hydroxyanthraquinone / Mucosal epithelium of large bowel / Apoptosis / Rat / ホスホリパーゼC / MAMacetate / azoxymethane / PCNA / I-hydroxyamthraquinone / アポトーシス / 大腸 |
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| Research Abstract |
Expression of cytokines was examined in methylazoxymethanol (MAM) acetate and/or 1-hydroxyanthraquinone (1-HA)-induced large bowel neoplasms and carcinogen exposed non-neoplastic epithelium of the bowel in rats. Both cytokines of TNF-a and IL-la was more expressed in the carcinogen-initiated non-neoplastic epithelium than in the normal epithelium. The expression of the cytokines in the neoplasms was stronger than in the non-neoplastic epithelium. The results suggest a mutual relationship between the expression of the cytokines and carcinogenesis.
Arachidonic acid is induced by activation of phospholipase C (PLC) as well as phospholipase A_2. We discovered that expression of PLC-delta, one of 3 isozymes of PLC of the neoplasms is lower than of the non-neoplastic tissues in the large bowel carcinogenesis of rats. These results also imply that expression of imflammation associated enzymes and cytokines is related to cell growth or carcinogenesis in the large bowel.
Relationship between the cell proliferation and the apoptosis was investigated in mucosal epithelium of large bowel on the initial stage of azoxymethane-induced carcinogenesis. Apoptosis was induced 4 hours after the exposure of carcinogen and reached to the peak at after 8 hours. In 3 days, appearance of apoptosis was decreased and increased the cell proliferation reversely. AOM-induced apoptosis appeared to relate to inhibition of mitosis. PCNA was found to be not the biomarker for cell proliferation in the early stage of AOM-induced toxicity which is associated with cell-cycle arrest.
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