论文部分内容阅读
野生型 -p5 3 (wt-p5 3 )作为关卡基因在DNA受损伤时使细胞停止在G1期 ,使受损细胞修复或发生细胞凋亡。本研究利用RT -PCR法研究高Zn2 + 、缺Zn2 + 作用 2 4小时后对鼠胶质瘤细胞wt-p5 3mRNA表达的影响。取对数生长期的鼠胶质瘤细胞 ,在RPMI - 1640常规培养液中分别加入 0 3mmol L的Zn2 + 和5 μmol L的TPEN培养 2 4h后发现 0 3mmol L的Zn2 + 作用 2 4小时抑制鼠胶质瘤细胞wt-p5 3表达 ,5 μmol L的TPEN作用 2 4小时鼠胶质瘤细胞wt -p5 3mRNA表达水平升高。这表明高Zn2 + 抑制鼠胶质瘤细胞wt -p5 3RNA表达 ,缺Zn2 + 可提高鼠胶质瘤细胞wt-p5 3mRNA表达水平
As a checkpoint gene, wild-type-p5 3 (wt-p5 3) stops cells in the G1 phase when DNA is damaged, repairing damaged cells or causing apoptosis. In this study, RT-PCR was used to study the effects of high Zn2 + and Zn2 + on the expression of wt-p5 3 mRNA in glioma cells after 24 hours. Logarithmic growth phase glioma cells were treated with 0 3 mmol L of Zn2 + and 5 μmol L of TPEN for 24 h in RPMI - 1640 conventional culture medium. After 24 h incubation with 0 3 mmol L of Zn2 +, 24 h inhibition was observed The expression of wt-p5 3 in glioma cells and the expression of wt-p5 3 mRNA in 24 h glioma cells increased with TPEN induced by 5 μmol L. This indicates that high Zn2 + inhibits the expression of wt-p5 3RNA in glioma cells, while the absence of Zn2 + can increase the expression of wt-p5 3 mRNA in glioma cells