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MOLECULAR MECHANISM OF INFLAMMATORY AND IMMUNOLOGICAL FACTORS INVOLVED IN DRUG-INDUCED LIVER INJURY

Research Project

Project/Area Number 09672209
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Biological pharmacy
Research InstitutionShowa Pharmaceutical University

Principal Investigator

HOJO Hiroshi  FACULTY OF PHARMACEUTICAL SCIENCES, DEPT. OF HYGIENIC CHEMISTRY, SHOWA PHARMACEUTICAL UNIVERSITY, 薬学部, 教授 (90004621)

Project Period (FY) 1997 – 1999
Project Status Completed (Fiscal Year 1999)
Budget Amount *help
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1999: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1998: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1997: ¥1,600,000 (Direct Cost: ¥1,600,000)
KeywordsLiver injury / carbon tetracloride / interleukin-6 / cytokine / rat / dexamethasone / インターロイキン6 / デキサメサゾン / エンドトキシン
Research Abstract

We have investigated the role of inflammatory and immune mediators in the carbon tetrachloride induced liver injury models. An administration of carbon tetrachloride through the subcutaneous (s.c.) or intraperitoneal (I.p.) route induced interleukln-6 (IL-6) in plasma with a peak at 8 and 4 hr later, respectively, but that through the per os (p.s.) route did not. The maker hepatic enzyme activities were increased with a peak 24 hr to 48 hr after carbon tetrachloride administration, however, the rate of increase was higher through the p.o. route than through the s.c. or I.p. route. As ratios of the vehicle (corn oil) to carbon tetrachloride were increased, the IL-6 induction was decreased and the leak of hepatic enzymes was augmented. Pretreatment with dexamethasone markedly suppressed the IL-6 induction and enhanced the enzyme leaks in the rats treated with carbon tetrachloride through the s.c. or I.p. route.
These results represent the close reverse correlation between IL-6 induction and liver injury, suggesting the IL-6 induced in the early phase after carbon tetrachloride might play a suppressive role in the development of the liver injury.

Report

(4 results)
  • 1999 Annual Research Report   Final Research Report Summary
  • 1998 Annual Research Report
  • 1997 Annual Research Report
  • Research Products

    (3 results)

All Other

All Publications (3 results)

  • [Publications] M. Yamaguchi, D. Kambayashi, J. Toda, T. Sato, S. Toyoshima, H. Hojo: "Acetylleucine chloromethyl ketone, an inhibitor of acetylpeptide hydrolase, induces apoptosis of U937 cells"Biochemical and Biophysical Research Communications. 263・1. 139-142 (1999)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] M.Yamaguchi, D.Kambayashi, T.Toda, T.Sano, S.Toyoshima and H.Hojo: "Acetylleucine chloromethyl ketone, an inhibitor of acylpeptide hydrolase induces apoptosis of U937 cells"Biochemical and Biophysical Research Communications. 263. 139-142 (1999)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1999 Final Research Report Summary
  • [Publications] M. Yamaguchi, D. Kambayashi, J. Toda, T. Sang, S.Toyoshima, H. Hojo: "Acetylleucine chlorine Hyl ketene, an inhibition acetylteltide hyctrolase, induces apoptosis of U937 cells"Biochemical and Biophysical Research Communications. 263.1. 139-142 (1999)

    • Related Report
      1999 Annual Research Report

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Published: 1997-04-01   Modified: 2016-04-21  

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