中文摘要：

目的：通过探讨HL-60细胞被TNF-α激活后NF-κB及IκBα活化的改变,了解银杏叶提取物（GbE）在治疗哮喘中部分可能的分子机理。方法：以HL-60细胞作为工具细胞,分別经TNF-α、GbE刺激,转染带有报告基因的质粒pNF-κB-Luc,通过荧光素酶的表达情况检测NF-κB活性变化;用免疫印迹方法检测IκBα的活化状况。结果：检测结果显示,以GbE预处理HL-60细胞可以明显抑制TNFα诱导的NF-κB转录激活的活性;但用GbE预处理细胞并不能拮抗TNF-α诱导的IκBα的磷酸化和降解,将GbE处理细胞时间延长和加大GbE的浓度同样不能阻止IκBα的磷酸化和降解。结论：GbE能抑制NF-κB激活的基因转录但并不是通过干扰经典的NIK/IKK/IκBα活化途径,而是通过干扰其它途径或采用其它方式来实现的。

英文摘要：

Objective：To investigate NF-KB and IκBα activities in HL-60 induced by TNF-α in order to understand the molecular mechanism of GbE in asthma treatment. Methods ：The amount of IκBα in HL-60 cells stimulated by TNF-α and GbE was measured by western blotting. Plasmid pNF-κB-Luc was transfected and NF-κB activity was analyzed by measuring the expression level of luciferase. Results ： It showed in the luciferase assay that the activity of NF-κB could significantly be suppressed in HL-60 cells after the pretreatment with GbE. However, the phosphory-lation and subsequent degradation, of IκBα induced by TNF-α cancnot be inhibited in HL-60 ceils even we prolonged the treatment time or increased the concentration of GbE. Conclusion：GbE can suppress the NF-κB gene expression actively on independent of NIK/ IKK/ IκBα pathway in HL-60 cells.