肿瘤坏死因子α通过NF—kB上调HepG2细胞中蛋白酪氨酸磷酸酶1B的表达  

TNF-α up-regulates protein tyrosine phosphatase 1B via NF-kB in HepG2 cells

作　　者：吴捷[1] 邹大进[1] 王淼[1] 郭献灵[1] 张丽娟[1] 吴鸿[1] 卢斌[1] 陈月[1] 

机构地区：[1]第二军医大学附属长海医院内分泌科,上海200433

出　　处：《中华内分泌代谢杂志》2009年第3期326-328,共3页Chinese Journal of Endocrinology and Metabolism

摘　　要：用不同浓度的肿瘤坏死因子α（TNF-α）诱导人肝癌细胞（HepG2细胞），结果表明TNF—α上调HepG2细胞蛋白酪氨酸磷酸酶1B（PTP-1B）的表达，激活NF—kB，并呈浓度依赖性，抑制NF-kB能阻断TNF—α对HepG2细胞PTP-1B的L凋作用。提示TNF—α可能通过激活NF—kB从而诱导HepG2细胞PTP-1B表达的上调。HepG2 cells were treated with various concentrations of tumor necrosis factor-α（TNF-α） for 24 hours. RT-PCR and Western blot were used to measure protein tyrosine phosphatase-1 B（ PTP-1B）expression, anti luciferase reporter assay was used to detect NF-kB activity. The results showed that treatment of HepG2 cells with TNF-α for 24 hours led to upregulation of PTP-1B and NF-kB activity in a dose-dependent manner. Inhibition of NF-kB by PDTC significantly attenuated TNF-α-induced PTP-1B expression in HepG2 cells. Thus, the transactivation of NF-kB seems to play an important role in the expression of PTP-1B in HepG2 cells induced by TNF-α .

关 键 词：蛋白酪氯酸磷酸酶1B 肿瘤坏死因子Α HEPG2细胞 NF—kB 

分 类 号：R346[医药卫生—基础医学]