X射线诱导人滋养细胞周期及凋亡改变的研究

目的:观察X射线对人滋养细胞JEG-3肿瘤细胞株的生物学特性的影响及作用。方法:体外培养人滋养细胞肿瘤细胞系(JEG-3细胞),采用不同剂量的X射线(2Gy、6Gy、8Gy)照射JEG-3细胞,MTT法测定照后不同时间(12、24、36h)的细胞增殖能力;流式细胞术检测6Gy照后不同时间(12、24、36h)的细胞凋亡的变化;western-blot检测P53、Bcl-2蛋白的表达量的变化。结果:6GyX射线照后36h细胞增殖活性下降;8Gy照后对细胞产生了明显的毒性,照后12、24、36h时细胞增殖均明显下降(P0.05)。6Gy照后36h时凋亡率显著增加(P0.05)。6Gy照后36h,凋亡相关蛋白P53的蛋白表达量显著增加、Bcl-2的蛋白表达量显著降低(P0.05)。结论:6GyX射线照射可抑制人滋养细胞的增殖,提高细胞凋亡率;同时诱导P53蛋白表达增加和Bcl-2表达降低。

The research of X-ray on cell apoptosis and cycle of JEG-3cells

Objective： To abserve the effect of the X-ray to the biological characteristics of JEG-3 tumor celllines. Methods： The choriocaracinoma- trophoblast cell line （JEG-3） were cultured in vitro,exposured to X-ray of different doses（2Gy,6Gy,8Gy） to mimic a cell model. Afterfor 12,24 and 36h , the cell viability was examined by MTT assay; After exposured to 6Gy X-ray for 12,24,36h,the cell cycle and apoptosis rate were detected by flow cytometry;Western-blot was used to detect the protein of P53 and Bcl-2.Resuhs： There seems to be a downward trend After treated with 4Gy X-ray for 12,24,36h. After treated with 6Gy, the cell proliferation was decreased at different time points, especially at 36h was significantly（P〈0.05 ）After treated with 8Gy X-ray,for 12,24 and 36h, which produced obvious toxicity and the cell viability decreased sig- nificantly （P〈0.05）.6Gy was selected as the right dosage in the next experiments, construct the model successfully. Exposure to X-ray（6Gy）for 36h.And the cells treated with 6Gy show a increasing apoptosis at 36h（P〈0.05 ）. Exposure to X-ray（6Gy） for 36h, the protein expression of P53 was significantly increased, while the expression of Bcl-2 was decreased significantly（P〈0.05）.Conclusion： After treated with 6Gy X-ray, asuit- able cell oxidative stress model has been successfully established in trophoblast cells. After a dose of X-ray inhibits the proliferation of trphoblast cell, extend the G2/M phase and increased cell apoptosis rate. At the same timethe protein expression of P53 was increased, while the expres- sion of Bcl-2 was decreased.