中文摘要：

为了观察旋覆花内酯（1-O-acetylbritannilactone，ABL）乙酰化衍生物ABLO，对脂多糖（lipopolysaccharide，LPS）／干扰素-γ（interferon-γ，IFN-γ）刺激的内皮细胞ECV304活化及其与RAW264．7单核／巨噬细胞相互作用的影响，采用Western印迹检测核因子-κB（nuclearfactor-κB，NF-κB）活化以及NF-κB依赖的黏附分子的表达水平，应用电泳迁移率改变分析（electrophoretic mobility shiftassay，EMSA）检查ABLO2预处理及LPS/IFN-γ诱导对NF-κB与DNA结合活性的影响。结果显示，ABLO2显著抑制LPS／IFN-γ诱导的NF-κB核转位和DNA结合活性，同时ABLO2降低NF-κB抑制蛋白（IκB）激酶（IκB kinases，IKK）的活性，抑制IKB的磷酸化及降解；ABLO2还通过减少血管细胞黏附分子-1（vascular cell adhesion molecule-1，VCAM-1）、骨桥蛋白（osteopontin，OPN）、基质金属蛋白酶-9（metalloproteinase-9，MMP-9）、黏蛋白-C（tenascin-C）的表达，进而减弱单核细胞与内皮细胞之间的黏附作用。研究结果表明，ABLO，通过抑制IKK活性及IκB降解而抑制NF-κB活化，进而起到抑制NF-κB依赖的黏附分子表达及细胞黏附作用。

英文摘要：

To investigate the effects of 1,6-O2-diacetylbritannilactone （ABLO2） on the activation of endothelial cell ECV304 and its interaction with macrophages treated with lipopolysaccharide （LPS）/interferon- （IFN-γ）. Western blot analysis was adopted to measure the nuclear translocation of nuclear factor-κb （NF-κB） and the expression of some adhesion molecules. Electrophoretic mobility shift assay （EMSA） was used to detect DNA- binding activity of NF-κB in ECV304 cells pretreated with ABLO2. The results showed that ABLO2 inhibited the NF- κB activation by blocking Ir, B kinase （IKK） activation, and suppressing inhibitor of NF-κB （I-κB） phosphorylation and degradation. In addition, ABLO2 could inhibit the adhesion between endothelial cells and macrophages by decreasing the expression of vascular cell adhesion molecule-1 （VCAM-1）, osteopontin （OPN）, matrix metalloproteinase-9 （MMP-9） and tenascin-c. These results suggest that ABLO2 is a potent agent to prevent vascular inflammatory disease in the vessel.