| Project/Area Number |
11670414
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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 |
Legal medicine
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| Research Institution | Sapporo Medical University (2000-2001)
Kyoto University (1999) |
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Principal Investigator |
MATSUMOTO Hiroshi Department of Legal Medicine, Sapporo Medical University School of Medicine Professor, 医学部, 助教授 (60263092)
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| Co-Investigator(Kenkyū-buntansha) |
福井 有公 京都大学, 医学研究科, 教授 (10025588)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2000: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | ethanol / signal transcription / NF-kappaB / AP-1 / HIF-1 / rat / liver / heart / エンドトキシン / 類洞内皮細胞 / CREB / Kupffer 細胞 / nitric oxide |
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| Research Abstract |
● Ethanol activates NF-kappaB, but reduces activation of AP-1 60 min after loading in rat hepatocytes, perfused rat livers, and in vivo rat liver.
● In the alcohol liver injury rat model, activation of NF-kappaB occurs in liver, which activity is in correspondence with liver histopathology, cytokine expressions, and so on.
● Ethanol activates NF-kappaB in rat hepatocytes, which activity is higher than that induced by LPS.
● Ethanol reduced activation of NF-kappaB by LPS, where the inhibition of degradation by acetaldehyde contributed.
● In vivo ethanol bolus administration caused activation of NF-kappaB and AP-1 in both the heart and liver of Wistar rat.
● In vivo ethanol administration causes delay of activation of HIF-1alpha in rat heart, indicating that alcohol consumption may induces ischemic heart disease.
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