| Project/Area Number |
08670635
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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 |
Gastroenterology
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| Research Institution | Kansai Medical University |
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Principal Investigator |
NAITOH Yuji Kansai Medical University, Department of Medicine, Assistant Professor, 医学部, 講師 (30198014)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAZAKI Hiroaki Kansai Medical University, Department of Medicine, Assistance, 医学部, 助手 (30268370)
SEKI Toshihito Kansai Medical University, Department of Medicine, Assistant Professor, 医学部, 助教授 (70163087)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1996: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Peripheral-Type Benzodiazepine Receptor / Hepatic Encephalopathy |
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| Research Abstract |
To investigate the possible role of peripheral-type benzodiazepine receptors (PBR) in hepatic encephalopathy, we examined expression of PBR in mouse brain following thioacetamide (TAA) -induced acute liver failure. Treatment of mice with TAA resulted in an increase in the number of the binding sites of the PBR ligand tritium-labeled Ro5-4864 to brain homogenates, with no significant change in affinity of the ligand. The order ofpotency of different ligands to compete against tritium-labeled Ro5-4864 binding in the brain of TAA-treated mice was Ro5-4864 > PK11195 > diazepam > protoporphyrin IX,findings similar to those in the control. Northern blot analysis revealed an increase in PBR/isoquinoline binding protein (PBR/IBP) mRNA in mouse brain following TAA treatment, in a time-and dose-dependent manner. These results indicate that the increased number of PBR in the brains of TAA-treated mice relates to the induction of PBR/IBP expression and suggest that the induction of PBR in brain may contribute to pathogenesis of hepatic encephalopathy.
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