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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 investigate the mechanism of apoptosis induced by p38MAPK gene in C6 rat glioma cells. Methods The p38MAPK gene was introduced into C6 cells by liposome-mediated method. The changes of sTNF-α in the cell culture medium were detected by sandwich ELISA. The changes of membrane TNF-α and membrane TNFRI were detected by flow cytometry. Results After transfection of pCMV5-p38MAPK, the level of sTNF-α in the cell culture medium was significantly increased, but there was no significant change in the membrane TNF-α level and the expression of membrane TNFRI was increased. Conclusion p38MAPK may induce apoptosis of C6 cells by up-regulating the levels of sTNF-α and membrane TNFRI.