四氯化碳肝纤维化大鼠储脂细胞表皮生长因子受体的变化  

Changes of Epidermal Growth Factor Receptor of Fat～storing Cells in CCl_4～induced Hepatofibrosis in Rats

作　　者：刘海林[1] 李宣海[2] 杨少平[2] 王丹艺[2] 

机构地区：[1]上海第二医科大学附属第九人民医院消化内科,200011 [2]上海第二医科大学

出　　处：《胃肠病学》1999年第3期161-162,共2页Chinese Journal of Gastroenterology

基　　金：上海市科委自然科学基金!95ZB14003;上海市教委科学技术发展基金!96B06

摘　　要：目的：研究四氯化碳（ＣＣｌ_４）所致实验性肝纤维化大鼠肝脏储脂细胞（ＦＳＣ）表皮生长因子受体（ＥＧＦ－Ｒ）的变化，探讨ＥＧＦ－Ｒ在ＦＳＣ激活中的作用。方法：^（１２５）Ｉ标记ＥＧＦ，放射配体结合分析测定正常和ＣＣｌ４肝纤维化大鼠肝脏原代ＦＳＣ的ＥＧＦ－Ｒ　结果：ＣＣｌ４肝纤维化大鼠肝脏ＦＳＣ数量（６．７１× １０~±５．３２ × １０~７）较正常大鼠（２．６３×１０~７±１．０４×１０~７）显著增多（Ｐ＜０．０５）；正常与 ＣＣｌ_４肝纤维化大鼠ＦＳＣ的ＥＧＦ－Ｒ最大结合位点数（ＲＴ）、解离常数（ｋＤ）分别为：２．２２ ×１０~３ｓｉｔｅｓ／ｃｅｌｌ，４．０９ × １０~(－１０）Ｍ和９．２７× １０~３ｓｉｔｅｓ／ｃｅｌｌ，３．２６× １０~(－１０）Ｍ。肝纤维化时ＥＧＦ－Ｒ明显增高（Ｐ＜０．０５）。结论：ＣＣｌ_４引起肝纤维化时ＦＳＣ增殖，同时ＥＧＦ－Ｒ的表达增加。Background/Aims: To investigate the changes of epidermal growth factor receptor(EGF-R) in CCl_4-induced hepatofibrosis in rats, and the role of EGF～R in activation of fat-storing cells(FSC). Methods: Using ^(125)I labeled EGF, the EGF～R of FSC was determined by radioligand binding assay. Results: The amount of FSC in CCl_4-induced fibrotic liver of rats increased significantly(p<0.05); the maximum binding sites of EGF-R and kD in FSC isolated from normal and fibrotic liver of rats were 2.22 × 10_3sites/cell, 4.09 × 10^(-10)M and 9.07 × 10~3 sites/cell, 3.26 × 10^(-10)M, respectively. The expression of EGF-R of FSC increased markedly in hepatofibrosis(P<0.05). Conclusions: FSC proliferation is promoted remarkably in CCl_4～induced hepatofibrosis in rats and the expression of EGF-R is also enhanced markedly.

关 键 词：肝纤维化大鼠 EGF-R 脂细胞 鼠肝 表皮生长因子受体 肝脏 四氯化碳 FSC 增加 最大 

分 类 号：R575.2[医药卫生—消化系统] R285.5[医药卫生—内科学]