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[目的]通过研究甲基汞对人胚胎神经干细胞mi RNA表达的影响,探讨低剂量甲基汞对神经干细胞细胞周期调控基因的调节作用。[方法]以0、10、50 nmol/L甲基汞染毒人胚胎神经干细胞24 h后,用MTT法测定甲基汞对细胞活力影响,应用逆转录多聚酶链反应(RT-PCR)检测甲基汞对细胞周期调控基因(p16、p21)的m RNA的表达水平影响,利用实时荧光定量多聚酶链反应技术检测调控p16、p21的mi RNA(mi R-24、mi R-106a)的表达情况。[结果]50 nmol/L甲基汞染毒组细胞活力降低为对照组的53.5%,差异有统计学意义(P<0.05);p16与p21基因的m RNA表达水平随着甲基汞染毒浓度的升高而升高,差异均有统计学意义(P<0.05),但10 nmol/L与50 nmol/L组的p16基因表达差异无统计学意义。mi R-24、mi R-106a的表达水平随着甲基汞染毒浓度的升高而降低,差异有统计学意义(P<0.05)。[结论]50 nmol/L的甲基汞可以引起人胚胎神经干细胞增殖抑制,并可能通过mi RNA调节细胞周期调控基因的表达。
[Objective] To investigate the effect of methylmercury on miRNA expression in human embryonic neural stem cells and to investigate the regulatory effect of low dose methylmercury on the cell cycle regulatory genes of neural stem cells. [Methods] After the human embryonic neural stem cells were treated with 0, 10 and 50 nmol / L methylmercury for 24 h, MTT assay was used to determine the effect of methylmercury on cell viability. RT-PCR was used to detect the effect of methylmercury Effect of Mercury on the Expression of m RNA in Cell Cycle Regulatory Genes (p16, p21) Using Real-time Fluorescent Quantitative Polymerase Chain Reaction to Detect the Expression of mi R-24 and mi R-106a Regulating the Expression of p16 and p21 . [Results] The cell viability in 50 nmol / L methylmercury-treated group was reduced to 53.5% of that in control group (P <0.05). The m RNA expression levels of p16 and p21 were significantly different with those of methylmercury (P <0.05). However, there was no significant difference in p16 gene expression between 10 nmol / L and 50 nmol / L groups. The expression of mi R-24 and mi R-106a decreased with the increase of methylmercury exposure, the difference was statistically significant (P <0.05). [Conclusion] 50 nmol / L methylmercury can induce the proliferation inhibition of human embryonic neural stem cells, and may regulate the expression of cell cycle regulatory genes through miRNA.