硝普钠抑制脂多糖诱导的大鼠原代培养肝细胞表面细胞间粘附分子-1的表达  

Sodium nitroprusside inhibits the expression of intercellular adhesion molecule-1 induced by lipopolysaccharide in primary cultured rat hepatocytes

作　　者：陈奕[1] 楼宜嘉[1] 王红莉[1] 

机构地区：[1]浙江大学药学院药理与毒理学研究室,浙江杭州310031

出　　处：《中国药理学与毒理学杂志》2003年第4期266-269,共4页Chinese Journal of Pharmacology and Toxicology

基　　金：国家自然科学基金资助 ( 30 0 70 90 4 )~~

摘　　要：目的　评价模拟肝脏急性炎症期一氧化氮与细胞间粘附分子 1(ICAM 1)表达的关系。方法　用免疫细胞化学技术检测加入不同浓度NO供体硝普钠 (SNP)和 (或 )细菌内毒素 (LPS)后 ,原代培养大鼠肝细胞ICAM 1的表达情况。结果　当培养时间达4h ,各组肝细胞均未见ICAM 1显著表达 ;但当培养至 8,2 4h ,LPS组的肝细胞ICAM 1表达强度明显升高 (P <0 .0 5 ) ,SNP则可呈浓度依赖性地抑制LPS诱导的大鼠肝细胞ICAM 1的表达。结论　SNP可显著抑制LPS诱导的原代培养大鼠肝细胞ICAM 1表达。AIM To investigate the relation between nitric oxide (NO) and intercellular adhesion molecule 1 (ICAM 1) expression. METHODS The primary cultured rat hepatocytes were incuba ted with sodium nitroprusside (SNP), and the 50% lethal concentration (LC 50 ) was measured by microculture tetrazolium assay (MTT). The expression of ICAM 1 in hepatocytes was detected by immunocytochemistry when the cells were incubated with SNP in 0, 100, 200, and 300 μmol·L -1 alone, or lipopolysaccharide (LPS) 10 mg·L -1 +SNP in fresh media for 4, 8 or 24 h, respectively. RESULTS Exposure of hepatocytes to SNP for 24 h, the value of LC 50 and 95% confidence limits was 597 (532-670) μmol·L -1 . ICAM 1 positive hepatocytes in negative control were (3.1± 1.8)%, and in SNP groups were <(4.5± 2.2)%. ICAM 1 expression could be up regulated by LPS in hepatocytes positive cells (98.7± 2.6)% . SNP(100, 200, 300 μmol·L -1 ) could down regulated ICAM 1 overexpression stimulated by LPS to (68.6±3.4)%, (42.4±5.6)%, (20.1±1.8)% for 24 h incubation. CONCLUSION NO donor SNP can suppress ICAM 1 overexpression in primary cultured rat hepatocytes stimulated by LPS.

关 键 词：一氧化氮 肝细胞 原代 培养 粘附 

分 类 号：R965[医药卫生—药理学]