摘要
目的 初步探讨p38MAPK基因诱导大鼠胶质瘤细胞C6发生凋亡的机制。方法 利用脂质体介导法将p38MAPK基因导入C6细胞中,用夹心法ELISA检测细胞培养液中sTNF-α水平的变化,用流式细胞仪检测膜TNF-α和膜TNFRI水平的变化。结果 转染pCMV5-p38MAPK后,细胞培养液中sTNF-α水平明显升高,膜TNF-α水平无明显变化,膜TNFRI表达升高。结论 p38MAPK可能通过上调sTNF-α和膜TNFRI水平而诱导C6细胞凋亡。
Objective To study the mechanisms of the glioma cells apoptosis induced by p38MAPK gene in rats. Methods p38MAPK was transfected into C6 cells by lipofectin. The concentration of sTNF-cc in the culture fluid was determined by ELISA, antl the concentrations of membrane TNF-α and membrane TNFRI were determined by flow cytometry. Results The concentrations of the sTNF-α in the culture fluid and membrance TNFRI in the pCMV5-p38MAPK transfection group were significantly higher than those in the control group (P<0.01). The insignificant difference (P>0.05) in the concentration of the membrane TNF-α between the pCMV5-p38MAPK transfection and control groups was observed. Conclusion The increase in sTNF -α and TNFRI may be one of the mechanisms that p38MAPK induces the apoptosis of C6 cells in the rats.
出处
《中国临床神经外科杂志》
2002年第5期295-297,共3页
Chinese Journal of Clinical Neurosurgery
