论文部分内容阅读
目的研究亚砷酸钠对人正常膀胱上皮(SV-HUC-1)细胞中信号传导与转录激活因子3(STAT3)m RNA表达的影响。方法将处于对数生长期的SV-HUC-1细胞分别进行急性染毒[暴露于含终浓度为0(对照)、1、2、4、8、10μmol/L亚砷酸钠的培养基染毒24 h]和慢性染毒[以含终浓度为0(对照)、0.5μmol/L亚砷酸钠的培养基染毒40代]。采用逆转录PCR(RT-PCR)方法检测细胞STAT3 m RNA表达情况。结果与对照组比较,4、8、10μmol/L亚砷酸钠暴露组SV-HUC-1细胞内STAT3 m RNA的表达水平均升高,差异均有统计学意义(P<0.05);且随着亚砷酸钠染毒剂量的升高,SV-HUC-1细胞内STAT3 m RNA的表达水平呈先升高后下降的趋势。0.5μmol/L亚砷酸钠慢性暴露组SV-HUC-1细胞内STAT3m RNA的表达水平高于对照组,差异有统计学意义(P<0.05)。结论砷可能通过调控STAT3的表达而在砷诱导的SVHUC-1细胞恶性转化中发挥一定作用。
Objective To investigate the effect of sodium arsenite on the expression of signal transducer and activator of transcription 3 (STAT3) mRNA in human normal bladder epithelium (SV-HUC-1) cells. Methods Acute exposure to SV-HUC-1 cells in logarithmic growth phase [exposure to medium containing sodium arsenite at a final concentration of 0 (control), 1, 2, 4, 8, 10 μmol / Toxicity 24 h] and chronic exposure [to a culture medium containing 0.5 [mu] mol / L sodium arsenite at a final concentration of 0 (control) for 40 generations]. Reverse transcription PCR (RT-PCR) was used to detect STAT3 mRNA expression. Results Compared with the control group, STAT3 m RNA expression in SV-HUC-1 cells exposed to 4, 8 and 10 μmol / L sodium arsenite was significantly increased (P <0.05) With the dose of sodium arsenite increased, the expression level of STAT3mRNA in SV-HUC-1 cells firstly increased and then decreased. The level of STAT3mRNA in SV-HUC-1 cells exposed to 0.5μmol / L sodium arsenite was significantly higher than that in control group (P <0.05). Conclusion Arsenic may play a role in arsenic-induced malignant transformation of SVHUC-1 cells by regulating the expression of STAT3.