| Project/Area Number |
01570400
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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 |
Gastroenterology
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| Research Institution | Yamaguchi University School of Medicine Grant-in-Aid for Scientific Research (C) |
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Principal Investigator |
OKITA Kiwamu Yamaguchi University School of Medicine, Prof., 医学部, 教授 (70107738)
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| Co-Investigator(Kenkyū-buntansha) |
YASUNAGA Mitsuru Yamaguchi Univ. School of Med., Assis. Prof, 医学部附属病院, 助手 (90230234)
KONISHI Tomomi Yamaguchi Univ. School of Med., Assist. Prof, 医学部附属病院, 助手 (30195755)
FUKUMOTO Yohei Yamaguchi Univ. School of Med., Assoc. Prof., 医学部, 助教授 (90136193)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1990: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1989: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Liver Regeneration / Fulminant hepatitis / Epidermal Growth Factor (EGF) / EGF receptor / Acute-on-Chronic / Impaired Liver Regeneration / EPidermal Growth Factor(EGF) / 癌細胞増殖 / 上皮細胞増殖因子(EGF) / 肝再生調節因子 |
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| Research Abstract |
It is well-known that fulminant hepatitis is based upon severe hepatic cell necrosis. In this sense, this applicant has got the idea that promotion of liver regeneration might improve the mortality in this pathologic condition.
For these two years, we have mainly studied on how much Epidermal Growth Factor (EGF) can cause liver regeneration in this disease. First of all, we administered EGF into the rats carrying acute liver failure developed with CCl_4. Surprisingly, remarkable DNA synthesis could be induced in the liver after administration of EGF. Number of DNA synthesizing hepatocytes reached at maximum in case of its intra-portal administration, as compared with intra-peritoneal and intra-venous routes. On the other hand, we also investigated that EGF could stimulate DNA synthesis in the liver carrying acute liver failure on chronic liver injury (AOC) which has been known to be higher mortality than fulminant hepatitis. We developed animal model for AOC by means of administration of d-galactosamine into the animals with chronic liver injury induced with chronic treatment with CCl_4.
In conclusion, exogenously administered EGF never caused the increase of DNA synthesizing hepatocytes in this condition. Therefore, we can understand AOC is a condition of impaired liver regeneration.
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