摘要
目的探讨GSK-3抑制剂(Licl)治疗脑胶质瘤的可行性及其机制。方法于2015年1月—2015年6月期间将U251细胞经复苏处理后,经DMEM培养液并在接种后24 h达到连续传代对数生长期;分别将不同浓度的Li Cl作用于U251细胞24、48 h;并对比不同浓度与不同作用时间下细胞的存活率、细胞周期改变情况以及GSK-3β蛋白的表达情况。结果处理前,U251胶质瘤细胞的MTT值为1.0,不同浓度Li Cl作用U251胶质瘤细胞24 h后,MTT值下降为0.45,与处理前比较结果显示药物组的MTT值显著低于未处理组,差异有统计学意义,P<0.05,并呈剂量依赖关系。结论 Li Cl抑制剂能明显抑制胶质瘤U251细胞株的增殖,而且能上调GSK-3β蛋白的表达。
Objective To investigate the feasibility of GSK-3 inhibitor （Licl） and its mechanism of treating brain glioma. Methods During the period from January 2015 to June 2015 will be U251 cell recovery after treatment by DMEM medium and at 24 h after inoculation to continuous passage of the logarithmic growth phase; then different concentration of LiCl in U251 cells and 24h, 48h; comparison of cells at different concentrations and different action time on the survival rate, the changes of cell cycle and the expression of GSK-3 beta protein. Results Before treatment, U251 glioma cells MTT 1, different concentrations of LiCl in U251 glioma cells after 24 h, the MTT value decreased to 0.45, compared with the results before treatment showed drug group the MTT value was significantly lower than that in the untreated group, with statistical significance, P 〈 0.05, in a dose-dependent manner. Conclusion LiCl inhibitors can significantly inhibit the proliferation of U251 glioma cell lines, and can adjust the GSK-3 beta Protein expression.
出处
《中外医疗》
2016年第20期28-29,35,共3页
China & Foreign Medical Treatment
关键词
氯化锂
胶质瘤
增值
蛋白表达
Lithium chloride
Glioma
Proliferation
Expression
