1999 Fiscal Year Final Research Report Summary
The relationship between hepatic failure following hepatectomy and induction of apoptosis and its therapeutic approach
| Project/Area Number |
10671178
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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 |
Digestive surgery
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
YAMAMOTO Naritaka Kyoto University, Gastroenterological Surgery, Assistant Prof., 医学研究科, 助手 (30253298)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAOKA Yoshio Kyoto University, Gastroenterological Surgery, Professor, 医学研究科, 教授 (90089102)
SHIMAHARA Yasuyuki Kyoto University, Gastroenterological Surgery, Associate Prof, 医学研究科, 助教授 (30196498)
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| Project Period (FY) |
1998 – 1999
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| Keywords | hepatic failure / proliferative cholangitis / gene transfer / apoptosis |
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| Research Abstract |
We previously reported that blood levels of proinflammatory cytokines and adhesion molecules reflect the severity of underlying liver damage and that they change in response to the surgical stress during a perioperative period of hepatic surgery. Moreover, those levels were found to be significantly related to the occurrence of postoperative organ failures and the prognosis of the patients. In addition, the mRNA of IL-6 was recognized in peripheral mononuclear cells (PMNC) two hours after the start of the operation and increased in accordance with intraoperative bleeding volume and the severity of underlying liver damage. It was more induced in the liver tissues than in PMNC.In contrast, mRNA of ICAM-1 was more induced in PMNC than in the liver tissues, supporting a previous result that ICAM-1 appeared to be mainly produced in PMNC.In 1999, we established a method for a gene transfer using adenoviral vector or HVJ-liposome in a rat proliferative cholangitis model in order to apply the gene transfer technique in a clinical situation. We found that nonphosphorylatable retinoblastoma gene and E2F decoy, using adenovirus and HVJ-liposome, respectively, successfully inhibit the progress of proliferative cholangitis in rats. We are presently investigating possible involvement of apoptosis in this mechanism.
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