Project/Area Number |
13671342
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Digestive surgery
|
Research Institution | Keio University |
Principal Investigator |
SHIMAZU Motohide Keio University, School of Medicine, Assistant Professor, 医学部, 講師 (70124948)
|
Co-Investigator(Kenkyū-buntansha) |
SHINODA Masahiro Keio University, School of Medicine, Assistant, 医学部, 助手 (50286499)
TAKAYANAGI Atsushi Keio University, School of Medicine, Assistant, 医学部, 助手 (80245464)
|
Project Period (FY) |
2001 – 2002
|
Project Status |
Completed (Fiscal Year 2002)
|
Budget Amount *help |
¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2002: ¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 2001: ¥1,600,000 (Direct Cost: ¥1,600,000)
|
Keywords | IкB / NFкB / antisence / genetransfer / ischemia-reperfusion injury / liver transplantation / IkB / NFkB / 肝虚血再灌流傷害 |
Research Abstract |
NFкB is a transcriptional factor which plays a major role in production of inflammatory cytokines and regulation of apoptosis. However, it is still unclear whether up-regulation of NFкB has a cytoprotective effect or not in hepatic ischemia-reperfusion injury. We already constructed a recombinant adenovirus vector expressing a truncated form of the inhibition protein IкB (Adex IкB), and demonstrated that transfer of Adex IкB inhibited NFкB activation and aggravated hepatic ischemia-reperfusion injury in rats. In the present study, we tried to construct Adex IкB antisense suppressing IкB production and investigated the effect of IкB antisense gene transfer to NFкB activation and ischemia-reperfusion injury. In vitro, amount of IкB was not decreased in cultured cells infected Adex IкB antisense, although IкB antisense cDNA was detected by RT-PCR. In hepatic ischemia-reperfusion model in rats, administration of Adex IкB antisense did not attenuate hepatic injury compared to the control group
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