目的:研究氯化锂(LiCl)对人骨肉瘤细胞U2-OS增殖及凋亡的影响,并探讨其可能的机制.方法:以40、80、150 mmol/L的LiCl作用于U2-OS细胞24、48和72 h后,采用 MTT法检测细胞增殖抑制率;作用48 h后,流式细胞术法检测细胞凋亡率,并分析细胞周期;RT-PCR法检测凋亡相关基因Fas、Caspase-3 mRNA的表达.结果:随LiCl作用剂量的增加,U2-OS细胞增殖抑制率增加,细胞凋亡率和Fas、Caspase-3 mRNA表达量亦增加(F=61 157.480,70.828和418.072,P<0.001);细胞周期分析显示细胞被阻滞于S期(P<0.001).结论:LiCl可能通过促进凋亡基因Fas、Caspase-3的表达,抑制U2-OS细胞增殖并诱导凋亡.%Aim: To investigate the effect of lithium chloride( LiC) on proliferation and apoptosis of human osteosarco -ma cell U2-0S,and probe the possible mechanism. Methods: U2-OS cells were cultured with different concentrations of LiCl (40 ,80, and 150 mmol/L) for 24,48, and 72 h, respectively, then the growth inhibitory effects were detected with MTT. Apoptosis and cell cycle was observed by flow cytometry ,and Fas and Caspase-3 mRNA expression, by RT-PCR for cells cultured for 48 h. ReSUltS; LiCl could inhibit the growth of U2-OS cells, induce apoptosis ( F = 61 157. 480, P < 0.001) in a dose-dependent manner. The cell cycle analysis revealed that the cells were arrested in S checkpoint . LiCl could increase the expression of Fas and Caspase -3 mRNA obviously (F = 70. 828 ,418. 072 ,P < 0. 001). Conclusion : LiCl could inhibit the proliferation and induce apoptosis of U 2-OS cells through increasing the expression of Fas and Caspase -3.
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