中文摘要：

目的 探讨环境类致癌因子对调控成骨肉瘤细胞中胰岛素样生长因子2（insulin—like growth factor 2，IGF．2）基因表达的作用机制。方法应用环境类致癌因子二噁英（TCDD）作用于人成骨肉瘤细胞（SaOS-2）细胞株；采用流式细胞仪检测TCDD对SaOS-2细胞凋亡的影响规律；采用实时定量PCR定量分析SaOS-2细胞中IGF-2mRNA的表达；采用Western印迹杂交鉴定SAOS-2细胞中IGF-2和促分裂原活化蛋白激酶（MAPK）信号通路中的p38MAPK蛋白质的表达及磷酸化水平的变化。结果1×10^-9mol／L、1×10^-8mol／L、1×10^-7mol／L剂量的TCDD对SaOS-2细胞具有抗凋亡作用，在基因转录和翻译水平上增强SaOS-2细胞中IGF-2的表达；TCDD明显地降低了SaOS-2细胞内p38MAPK磷酸化水平。结论低生理浓度的TCDD可促进靶基因IGF-2的表达，并通过p38MAPK信号转导通路，发挥拮抗成骨细胞凋亡的毒性作用。

英文摘要：

Objective To investigate the regulation of environmental carcinogenic factor-2,3,7,8-tetrachlorodibenzo-p-dioxin （TCDD） on gene expression of insulin-like growth factor 2 （IGF-2） in osteogenie sarcoma （SaOS-2） cells. Methods Cell apoptosis in SaOS-2 cells treated with TCDD（ 1×10^-9 mol/L, 1 × 10 ^-8 mol/L, 1 × 10^-7 mol/L） was detected by flow cytometry. IGF-2 mRNA level in SaOS-2 cells was detected by real-time reverse transcription polymerase chain reaction （PCR）, and its protein and phosphorylation of p38 MAPK （mitogen-activated protein kinase） were detected by western blotting analysis. Results The rate of cell apoptosis treated with TCDD at 1 × 10^-9 mol/L, 1 ×10^-8 mol/L, 1× 10^-7mol/L concentration decreased about 5% , 26%and 52% , respectivily. Gene transcription and translation of IGF-2 were increased in TCDD-treated SaOS-2 cells. TCDD did not affect the protein expression of p38 MAPK in MAPK signal pathway, but down-regulated the phosphorylation tevel of p38 MAPK in SaOS-2 cells. Conclusion TCDD may be up-regnlated the gene expression of IGF-2 in SaOS-2 cells. The activity of p38 MAPK in SaOS-2 cells was inhibited by TCDD.