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本研究应用肿瘤细胞系在体外探讨锂是否直接诱导肿瘤细胞凋亡从而起到抑瘤作用.此外还观察了锂诱导细胞凋亡过程与蛋白质重新合成及第二信号传导系统的相关性,并检测了锂作用时p53,bcl-2和c-myc三种基因mRNA及蛋白水平的改变,以期进一步了解其作用机制.实验结果表明锂(LiCl)可以诱导人髓性细胞白血病细胞系HL-60、人单核细胞白血病细胞系U937及人卵巢癌细胞系A2780产生凋亡;表现出典型的凋亡特征,细胞形态皱缩,核固缩断裂.电泳可见明显的DNA“梯带”.在流式细胞分析仪显示在G_1峰前有凋亡特有的AP峰(Apoptotic Peak).诱导HL-60及U937凋亡的条件为1000μg/ml,LiCl,24小时,诱导A2780则需200μg/ml,48小时.
In this study, tumor cell lines were used to investigate whether lithium directly induced tumor cell apoptosis in vitro to inhibit tumors. In addition, lithium-induced apoptosis was correlated with protein synthesis and second signal transduction system. The effect of lithium on the mRNA and protein levels of p53, bcl-2 and c-myc were investigated in order to further understand the mechanism of action. The experimental results show that lithium (LiCl) can induce human myeloid leukemia cell line HL-60, The human monocyte leukemia cell line U937 and the human ovarian cancer cell line A2780 produce apoptosis; typical apoptotic characteristics are exhibited, cell morphology shrinks, and nuclear pyknosis breaks. The electrophoresis shows a distinct DNA “ladder”. The cell analyzer showed that there was apoptotic AP peak (Apoptotic Peak) in front of the G 1 peak. The conditions for inducing apoptosis of HL-60 and U937 were 1000 μg/ml, LiCl, 24 hours, and 200 μg/ml for A2780, 48 hours. .