摘要
目的 探讨丝裂素活化蛋白激酶 (mitogenactivatorproteinkinase ,MAPK)在三羟异黄酮 ( genistein)抗肿瘤血管生成中的作用。方法 以脐静脉内皮细胞 (ECV30 4 )为研究对象 ,通过四甲基偶氮唑盐 (MTT)实验检测三羟异黄酮和血管内皮生长因子 (vascularendothelialgrowthfactor,VEGF)对ECV30 4细胞增殖的影响 ,应用免疫细胞化学和激酶活性分析方法检测ECV30 4细胞MAPK磷酸化水平和激酶活性。结果 血管内皮生长因子 (vascularendothelialgrowthfactor,VEGF)单独处理能使ECV30 4细胞增殖 ,MAPK磷酸化水平和活性升高 ,而三羟异黄酮单独处理能抑制ECV30 4细胞增殖 ,MAPK磷酸化水平和活性降低 ,三羟异黄酮和VEGF同时处理时 ,细胞增殖受抑 ,MAPK磷酸化和MAPK激酶活性比VEGF单独处理组低 ,而比三羟异黄酮单独处理组高。结论 MAPK在三羟异黄酮抑制ECV30 4细胞增殖中发挥着重要作用 ,可能是三羟异黄酮抑制肿瘤血管生成的机制之一。
Objective To explore the role of mitogen activator protein kinase(MAPK) in tumor anti-angiogenesis by genistein.Methods To observe the effect of genistein on the proliferation of ECV304 cell with MTT methods.And to detect the level of the MAPK phosphorylation and the activity of the kinase in ECV304 cell with immunocytochemistry and kinase activity analysis methods.Results Vascular endothelial growth factor(VEGF) alone can facilitate the proliferation of ECV304 cells and up-regulate the phosphorylation and activity of MAPK.Whereas genistein alone can cause a restraint of proliferation,down-regulate the phosphorylation and activity of MAPK( P <0.01).The growth is still restrainted when being treated with genistein and VEGF together.The level of phosphorylation and the activity of MAPK fall down compared with VEGF alone treated group and up-regulate compared with genistein alone treated group.Conclusion MAPK is very important in the proliferation of ECV304 inhibited by genistein which maybe is one mechanism of anti-angiogenesis by genistein.
出处
《中国公共卫生》
CAS
CSCD
北大核心
2004年第11期1296-1298,共3页
Chinese Journal of Public Health
基金
国家自然科学基金 (30 0 0 0 1 36)
