2002 Fiscal Year Final Research Report Summary
Potential treatment for liver injury through suppression of activated Kupffer cells by PPAR γ
| Project/Area Number |
13670568
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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 | JIKEI UNIVERSITY SCHOOL OF MEDICINE |
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Principal Investigator |
OHATA Mitsuru JIKEI UNIVERSITY SCHOOL OF MEDICINE DEPARTMENT DEPARTMENT OF INTERNAL MEDICINE LECTURER, 医学部, 講師 (50231204)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMADA Seika JIKEI UNIVERSITY SCHOOL OF MEDICINE DEPARTMENT OF INTERNAL MEDICINE RESEARCH ASSISTANT, 医学部, 助手 (90297391)
TAKAHASHI Akira JIKEI UNIVERSITY SCHOOL OF MEDICINE DEPARTMENT OF INTERNAL MEDICINE RESEARCH ASSISTANT, 医学部, 助手 (70297399)
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| Project Period (FY) |
2001 – 2002
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| Keywords | PPARγ / Kuoffer cell / Liver injury / Transcriptional factor / Cytokine / TNFα / NFκ,B |
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| Research Abstract |
Female Sprague Dawley rats weighing about 300g were given ethanod (5g/kg BW) intragastncally, and were injected LPS 24h later.Liver injury was induced in this model.
Pioghtazone, the ligand for peroxisome proliferates-activated receptor gamma (PPARγ) prevented increase in plasma AST, ALT,and TNFα levels, but not affected on plasma and hepatic levels of lipid peroxide nor plasma endotoxin level in rats.
Pioghtazone also prevented hepatic inflammation and necrosis induced by ethanol and LPS.
Ethanol and LPS induction of TNFα mRNA in the liver were blunted by Pioghtazone, however, RXRα mRNA were not affected. PPARγ mRNA levels were suppressed by ethanol and LPS, but recaptured by pioghtazone.
These results suggest that pioghtazone may prevent liver injury induced by ethanol and LPS by suppression of TNFα mRNA at least partially through NFκ B pathway.
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