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Evaluation of hyaluronic acid as a marker of hepatic sinusoidal endothelial cell disorder in chronic liver injury

透明质酸作为慢性肝损伤肝窦内皮细胞紊乱标志物的评价

基本信息

批准号：
06670594
负责人：
UENO Takato
金额：
$ 1.15万
依托单位：
Kurume University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1995
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-06670594/
关键词：
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

项目摘要

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.

血清透明质酸（HA）主要被肝窦内皮细胞（SEC）降解。在肝硬化中，肝窦毛细血管化的发展减少了SEC中HA的结合和降解，导致高血清HA浓度。为探讨血清透明质酸（HA）水平是否可作为慢性肝损伤时SEC紊乱的一个有用指标，采用硫代乙酰胺（TAA）诱导大鼠慢性肝损伤模型，并以生理盐水作为对照。测定<14>TAA和对照组大鼠血清HA水平和肝组织中~（13）C-HA放射性。在TAA处理0、4、8、12和16周大鼠的SEC培养中，观察SEC的窗孔、抗CD 44的免疫荧光强度和^<14>C-HA结合量，发现血清HA水平和<14>肝组织中^ C-HA放射性随慢性肝损伤的进展而升高，肝硬化时最高。SEC中CD-44的数量、孔隙率和表达随慢性肝损伤的进展而降低，在肝硬化组最低。结果<14>表明，慢性肝损伤时血中HA浓度的升高主要是由于SEC的HA受体减少，从而导致与细胞结合的HA量减少所致。