摘要
背景与目的:抑制血管生成将为胶质瘤的治疗提供新的希望,本研究观测我室自行合成的化合物诺帝(Nordy)对人恶性胶质瘤细胞系U87细胞CXCR4表达及其功能活性的影响。方法:通过免疫荧光标记,激光共聚焦扫描显微术观测诺帝对U87细胞CXCR4表达的影响;采用鬼笔环肽(Phalloidin)-FITC标记丝状肌动蛋白(F-actin),并通过激光共聚焦扫描显微术观察诺帝对CXCR4活化引起的F-actin聚合的影响;分别采用趋化试验和酶联免疫吸附试验(ELISA)检测诺帝对CXCR4活化引起的细胞迁移活性增加和血管内皮生长因子(VEGF)分泌的影响。结果:25～100μmol/L诺帝处理12h可明显降低U87细胞中CXCR4的表达;用诺帝预处理细胞后,再加入间质细胞衍生因子(SDF-1α),结果发现诺帝可显著抑制CXCR4活化引起的U87细胞迁移活性增加、肌动蛋白聚合和促血管生成因子VEGF分泌。结论:抑制人恶性胶质瘤CXCR4的表达及功能活性可能是诺帝抗癌效应的机制之一。
BACKGROUND ＆ OBJECTIVE：Anti-angiogenesis could be one of the most promising strategies against gliomas. This study is designed to observe the effect of a compound Nordy on the expression and activity of CXCR4 in human glioblastoma cell line U87. METHODS： The expression of CXCR4 in U87 cells treated with or without Nordy was measured by indirect immunofluoreseence under confocal laser scanning microscopy. The effect of Nordy on CXCR4-induced actin polymerization, migration and VEGF production were detected by confocal laser scanning microscopy, chemokine assay and ELISA, respectively. RESULTS： The expression of CXCR4 in U87 cells was weakened after 25-100p, M Nordy treatment for 12h. CXCR4-induced actin polymerization, migration and VEGF production was also blocked by Nordy pretreatment. CONCLUSIONS： Inhibition of the expression and function of CXCR4 may account for one of the potential anti-cancer mechanisms of Nordy.
出处
《中国神经肿瘤杂志》
2007年第4期241-245,共5页
Chinese Journal of Neuro-Oncology
基金
国家自然科学基金资助项目(30670804)
"863"计划资助项目(2006AA02Z475)
