三氧化二砷复合物抑制人脑胶质瘤U87细胞生长的机制研究

Study on the Mechanism of Arsenic Trioxide Complex Inhibiting the Growth of Human Glioma Cell Line U87

关键词:  三氧化二砷复合物  人脑胶质瘤U87细胞  细胞凋亡  机制

Key words:  arsenic trioxide complex  human glioma U87 cells  cell apoptosis  mechanism

摘要:

目的 研究三氧化二砷复合物对人脑胶质瘤U87细胞凋亡的影响，并进一步探讨其作用机制。方法 采用激光共聚焦技术研究三氧化二砷各复合物进入细胞的方式；采用细胞划痕愈合试验观察其对U87细胞迁移能力的影响；采用血管形成试验观察其对新生血管形成能力的影响；流式细胞仪检测各组细胞周期及细胞凋亡；免疫蛋白印迹法检测凋亡相关蛋白Bcl-2、Bax和caspase-3的表达情况。结果 三氧化二砷复合物主要通过内吞方式进入细胞，能显著抑制U87细胞的迁移以及新生血管的形成；其可诱导U87细胞周期阻滞于G2/M期，促进细胞发生凋亡；三氧化二砷复合物促进Bax和caspase-3的表达，抑制Bcl-2的表达。结论 三氧化二砷复合物对U87细胞的抑制作用机制可能是通过内吞方式进入细胞后，上调Bax的表达，下调Bcl-2的表达，最终诱导细胞发生凋亡。

Abstract:

OBJECTIVE To study the effect of arsenic trioxide complex on the apoptosis of human glioma U87 cells and further explore its mechanism.METHODS Laser confocal method was used to study the way of arsenic trioxide complex entering cells. Cell scratch healing experiment was used to observe the effect on migration ability of U87 cells. Angiogenesis experiment was used to observe the ability of influencing neovascularization. Cell cycle and apoptosis were detected by flow cytometer. Immunoblotting method was used to detect the apoptosis related proteins of Bcl-2, Bax and caspase-3. RESULTS Arsenic trioxides mainly entered the cells by endocytosis, which could significantly inhibit the migration ability and neovascularization of U87 cells. Arsenic trioxides blocked the cell cycle of U87 cells at the G2/M phase, and promoted the early apoptosis of cells. Arsenic trioxides promoted the expression of Bax and caspase-3, and inhibited the expression of Bcl-2. CONCLUSION The inhibition mechanism of arsenic trioxide complex on U87 cells may be up-regulation of Bax expression and down-regulation of Bcl-2 expression after entering cells by endocytosis, leading to cell apoptosis.