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Molecular analysis of the mechanism of fibrosis in alcoholic liver disease

Research Project

Project/Area Number 07670624
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Gastroenterology
Research InstitutionTokyo Women's Medical College

Principal Investigator

TSUCHIYA Mariko  Tokyo Women's Medical College, Medicine, staff, 医学部, 助手 (00266826)

Co-Investigator(Kenkyū-buntansha) 栗原 毅  東京女子医科大学, 医学部, 講師 (90130252)
安部 康二  東京女子医科大学, 医学部, 助手 (90256553)
Project Period (FY) 1995 – 1997
Project Status Completed (Fiscal Year 1997)
Budget Amount *help
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1997: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1996: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
Keywordsalcoholic liver disease / liver cirrhosis / nitric oxide / nitric oxide synthase / heme oxygenase / heme oxygenase / 肝線維化 / コラーゲン / NOS / エンドトキシン / サイトカイン / hemoxygenase / 肝類洞
Research Abstract

In the pathogenesis of fibrosis in alcoholic liver injury, collagen may play a critical role in its process. We hypothesized in this study that type IV collagen might be a marker of angiogenetic transformation of sinusoidal structure. However, type I collagen dominantly changed in the fibrotic process, it was difficult to detect the small change of the expression of type IV collagen component.It may be preferable to use the cell culture system for the observation of the expression of type IV collagen.
In another aspect of liver fibrosis, several biological active substances, such as, nitric oxide (NO), carbon monoxide are involved in the pathophysiology of liver cirrhosis. These substances have multiple aspects relating to vasoactivity, cytokine-modulator and cell-proliferation etc., and are speculated to be contributing to various pathological mechanisms in a different manner. In this study, we investigated the changes of Nox on the loading of external endotoxin, and the mRNA expressio … More n of nitric oxide synthase (NOS) and heme oxygenase (HO) in the liver in several models of chronic liver injury. Alcoholic model (ALD) was induced by the administration of a liquid ethanol diet, and in cirrhotic model, rat was treated with thioacetamide for 8 weeks. HO-I mRNA was enhanced in both models comparing with control rat, and the expression was more intense in cirrhosis in the Northern analysis. Lipopolysaccharide (LPS) stimulated the HO-I expression of mRNA in ALD and cirrhotic animals. As to NOS mRNA expression, there were no significant changes in eNOS expression in both models, and jNOS was , not constantly, but detected in Northern and RT-PCR analysis, by LPS treatment.
Conclusion : 1) HO-I mRNA was induced in chronic liver injury, and was up-regulated by LPS stimulation, 2) the response of NO system was speculated to be counter-regulated toward HO system. In the process of chronic liver injury, biological substances and their synthase show different dynamics dependent of the primary disease. Less

Report

(4 results)
  • 1997 Annual Research Report   Final Research Report Summary
  • 1996 Annual Research Report
  • 1995 Annual Research Report
  • Research Products

    (3 results)

All Other

All Publications (3 results)

  • [Publications] 土谷まり子: "慢性アルコール投与ネットの微少循環構築の変化" 日本消化器病学会雑誌. 93. 251 (1996)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] Mariko Tsuchiya: "The structure of microcirculation in chronic alcoholic rat" Japanese Journal of Gastroenterology. 93. 251

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1997 Final Research Report Summary
  • [Publications] 土谷まり子: "慢性アルコール投与ラットの微小循環構築の変化" 日本消化器病学会雑誌. 93. 251 (1996)

    • Related Report
      1996 Annual Research Report

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Published: 1995-04-01   Modified: 2016-04-21  

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