大花旋覆花内酯通过抑制NF-κB活化抗血管炎症反应  

1-O-acetylbritannilactone inhibits vascular inflammatory response through suppressing NF-κB activation

作　　者：张佳[1] 尉坤[1] 刘月平[1] 温进坤[1] 张嫡群[1] 韩梅[1] 

机构地区：[1]河北医科大学基础医学研究所生物化学与分子生物学研究室,神经与血管生物学省部共建教育部重点实验室,河北石家庄050017

出　　处：《中国病理生理杂志》2008年第10期2033-2036,共4页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.30670845);河北省自然科学基金资助项目(No.C2007000831)

摘　　要：目的:以离体培养的血管环为研究对象,探讨大花旋覆花内酯(1-O-acetylbritannilactone,ABL)抑制脂多糖(LPS)诱导的血管炎症反应效应和分子机制。方法:将体外培养的血管环预先用ABL孵育后,再用LPS刺激,提取组织总蛋白进行Western blotting分析。结果:ABL抑制LPS诱导的IKK磷酸化活化和由此引发的IκBα的磷酸化降解,降低NF-κB水平,进而抑制NF-κB依赖的炎症因子iNOS、COX-2、ICAM-1和VCAM-1的表达。结论:ABL是一种调节NF-κB活性的制剂,具有抑制致炎因子表达,上调抑炎因子水平,维持两者平衡的作用,可消除LPS诱导的血管炎症反应。AIM： To investigate the effects and molecular mechanism of 1 -O -acetylbritannilatone （ABL） on LPS -induc, ed inflammatory responses in aorta in vitro. METHODS ： The aorta loops pretreated with ABL were stimulated with LPS for different times. The protein extracts from the aorta were used to detect the expression of inflammatory factors by Western blotting. RESULTS： ABL inhibited the activation of NF - κB and the expression of inflammatory factors iNOS, COX -2, ICAM - 1 and VCAM - 1 , and increased the level of anti - inflammatory factor IκBα via blocking the phosphorylation activation of IKK and the degradation of IκBα induced by LPS. CONCLUSION： ABL abolishes the vascular inflammatory response to LPS stimulation through modulating NF - κB activity.

关 键 词：旋覆花内酯 炎症 主动脉 NF—κB 

分 类 号：R363[医药卫生—病理学]