中文摘要：

目的研究细胞外信号调节激酶（extracellular signal-regulated protein kinase,ERK）对肿瘤坏死因子-α（TNF-α）诱导内皮细胞β-1,4-半乳糖基转移酶-I（β-1,4-GalT-I）表达的调节作用。方法用不同浓度的TNF-α刺激人脐静脉内皮细胞（human umbilical vein endothelial cells,HUVECs）,并作用不同的时间,检测β-1,4-GalT-I表达变化;应用ERK通路抑制剂U0126预处理HUVECs,再用TNF-α刺激HUVECs,检测β-1,4-GalT-I的表达变化,并通过内皮-单核细胞黏附试验观察HU-VECs黏附能力的改变。结果 TNF-α诱导HUVECsβ-1,4-GalT-I表达增加,且具有剂量和时间依赖关系;U0126显著抑制TNF-α引起的HUVECsβ-1,4-GalT-I表达的上调及其黏附能力的上调。结论 ERK信号转导通路可能参与调节TNF-α诱导的内皮细胞β-1,4-GalT-I的表达,并影响内皮细胞的黏附能力。

英文摘要：

We aimed to investigate the role of extracellular signal-regulated protein kinase（ERK） in regulating the expression of β-1,4-galactosyltransferase-I（β-1,4-GalT-I） in human umbilical vein endothelial cells（HUVECs） stimulated by tumor necrosis factor（TNF-α）.Cultured HUVECs were stimulated by TNF-α at different concentrations,and for different times.By RT-PCR,we found that β-1,4-GalT-I expression in HUVECs was up-regulated by TNF-α on a concentration and time dependent manner.In another group,cultured HUVECs were pretreated by U0126,an inhibitor of ERK,and then stimulated by TNF-α.We found that U0126 could significantly suppress TNF-α-enhanced expression of β-1,4-GalT-I in HUVECs and adherence ability of HUVECs.Thus,we conclude that ERK signal transduction pathway may participate in regulating β-1,4-GalT-I expression in endothelial cells（EC） stimulated by TNFα and influence the adhesion ability of EC.