| Project/Area Number |
06670594
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Gastroenterology
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| Research Institution | Kurume University |
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Principal Investigator |
UENO Takato Kurume University School of Medicine, 2nd Department of Medicine, Assistant Prof., 医学部, 講師 (70176618)
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| Co-Investigator(Kenkyū-buntansha) |
TAMAKI Seishu Kurume University School of Medicine, 2nd Department of Medicine, Assistant, 医学部, 助手 (00258443)
TORIMURA Takuji Kurume University School of Medicine, 2nd Department of Medicine, Assistant, 医学部, 助手 (60197986)
INUZUKA Sadataka Kurume University School of Medicine, 2nd Department of Medicine, Assistant, 医学部, 助手 (80193572)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | liver injury / Sinusoidal endothelial cell / Hyaluronic acid / Hyaluronic acid receptor / CD-44 / Liver cirrhosis / 肝線維化 / 肝類洞内皮細胞 / C型慢性肝炎 / インターフェロン治療 |
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| Research Abstract |
Most of the serum hyaluronic acid (HA) is degraded by hepatic sinusoidal endothelial cells (SEC). In liver cirrhosis, the bindig and degradation of HA in SEC are considered to be reduced by development of hepatic sinusoidal capillarization, resulting in high serum HA concentration. The aim of this study is to clarify whether serum HA level is an useful marker of SEC disorder in chronic liver injury.
Chronic liver injury model rats were induced by thioacetamide (TAA) administration and control rats by physiologic saline. Serum HA levels and ^<14>C-HA radioactivity of liver tissues in TAA and control rats were measured. In cultured SEC obtained from 0,4,8,12 and 16-week TAA treated rats, 1) the observation of fenestrae in SEC.2) the immunofluorescent intensity of anti-CD44, and 3) the amount of ^<14>C-HA binding were determined.
Serum HA levels ad ^<14>C-HA radioactivity of liver tissues increased with progression of chronic liver injury, and were the highest in liver cirrhosis. The number, porosity and expression of CD-44 in SEC decreased with progression of chronic liver injury and were the lowest in liver cirrhosis. Moreover, the amount of ^<14>C-HA binding to SEC significantly decreased in liver cirrhosis compared with the controls.
These results indicate that the elevation of the blood HA concentration in chronic liver injury mainly occurs from a reduction in HA receptors of SEC and a consequent reduction in the amount of HA binding to the cells.
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