| Project/Area Number |
60570335
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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 | Osaka City University |
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Principal Investigator |
SAITO Shinobu (1986) Osaka City University Medical School, 医学部, 助手 (60162202)
東森 俊博 (1985) 大阪市立大学, 医学部, 助手
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| Co-Investigator(Kenkyū-buntansha) |
SAKAGAMI Yoshihide Osaka City University Medical School, 医学部, 助手 (40178546)
MIZOGUCHI Yasuhiro Osaka City University Medical School, 医学部, 講師 (00094491)
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| Project Period (FY) |
1985 – 1986
|
| Project Status |
Completed (Fiscal Year 1986)
|
| Budget Amount *help |
¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1986: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1985: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | acute hepatic failure / fulminant hepatitis / macrophage / hepatocytotoxic factor / 肝不全 |
|---|
| Research Abstract |
When heat-killed Propionibacterium acnes (P. acnes) is intravenously injected into mice and seven days later, a small amount of gram-negative lipopolysaccharide (LPS) is also intravenously injected, most of the mice die of massive necrosis. In this experimentally-induced acute hepatic failure, the adherent cells accumulated into the liver are primed by P. acnes and activated by LPS, producing the cytotoxic factor. This hepatocytotoxic factor is a protein-like substance and is relatively unstable to heat. Furthermore, in this experimentally-induced acute hepatic failure model, gomisin A, AA861, azelastine and prostaglandin <E_1> remarkably increase the survival rate of mice and improve the histological changes and necrosis of the liver cells.
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