Project/Area Number |
12670456
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Gastroenterology
|
Research Institution | THE UNIVERSITY OF TSUKUBA |
Principal Investigator |
SHODA Junichi Institute of Clinical Medicine, University of Tsukuba, Assistant Professor, 臨床医学系, 講師 (90241827)
|
Co-Investigator(Kenkyū-buntansha) |
SUZUKI Hiroshi Graduate School of Pharmaceuticak Sciences, University of Tokyo, 薬学部, 助教授 (80206523)
KAWAMOTO Toru Institute of Clinical Medicine, University of Tsukuba, Assistant Professor, 臨床医学系, 講師 (30282354)
|
Project Period (FY) |
2000 – 2002
|
Project Status |
Completed (Fiscal Year 2002)
|
Budget Amount *help |
¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2002: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2001: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2000: ¥2,600,000 (Direct Cost: ¥2,600,000)
|
Keywords | bilirubin / obstractive cholestasis / primary hepatolithiasis / hepatobiliary malignancy / biliary secretory mechanism / canalicular membrane transporter / bile acid / oxidative stress / 経皮経肝胆道ドレナージ / 輸送蛋白 / 胆汁うっ滞 / 脂質メディエーター / 炎症病態 / ホスホリパーゼAz / 血小板活性化因子 / PAF-AH / 肝輸送蛋白 |
Research Abstract |
The transport of biliary constituents across the canalicular membrane is the rate-limiting step in bile formation. Since long-standing biliary obstruction and complication of cholangitis associated with biliary infection have a large influence upon the hepatic secretory function through inflammation-related oxidative stress on the liver, interest should be focused on the expression levels of canalicular membrane transporter proteins in the cholestatic liver of patients with hepatobiliary diseases. We determined the molecular and immunohistochemical expression of canalicular transporter proteins, for bilirubin conjugate and bile acid,in the liver of patients with hepatolithiasis and in those of the patients with obstructive cholestasis who had undergone preoperative biliary drainage. Furthermore, their expression levels were correlated with the impairment of biliary secretion. This study concludes that in the liver of hepatobiliary diseases, the altered expression of the canalicular transporters may be associated with the impairment of bile formation and secretion, propably through inflammation-related oxidative stress on the liver.
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