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目的探讨氧化损伤相关基因硫氧还蛋白(TRX)、缺氧诱导因子-1(HIF-1)和血管内皮生长因子(VEGF)在镍致癌过程中作用。方法采用Ni2O3分别处理人胚肺成纤维细胞(WI-38)24,48和72 h。通过RT-PCR的方法检测TRX、HIF-1和VEGF基因mRNA的表达。结果Ni2O3处理24 h后,各浓度组(5,10和15μg/ml)VEGF基因mRNA表达〔(0.76±0.04),(0.78±0.06)和(0.69±0.01)(log cDNA/logβ-actin)〕均较对照组(0.58±0.02)上升(P<0.05)。48和72 h处理结果也较对照组升高。Ni2O3处理72 h后,各浓度组TRX基因mRNA表达〔(0.36±0.15),(0.31±0.07)和(0.31±0.02)〕均较对照组(1.06±0.09)下降(P<0.05)。5和10μg/ml Ni2O3组在作用48h后HIF-1基因mRNA表达水平〔(1.01±0.04)和(0.82±0.12)〕显著高于对照组〔(0.47±0.02),(P<0.05)〕,72 h后开始下降〔(0.66±0.10)和(0.69±0.13)〕;15μg/ml Ni2O3组(处理24,48和72 h)与对照组比较,差异无统计学意义。结论TRX、HIF-1和VEGF等与氧化损伤相关基因表达的改变可能在镍诱导细胞转化过程中起重要作用。
Objective To investigate the role of oxidative damage-related genes (TRX), hypoxia-inducible factor-1 (HIF-1) and vascular endothelial growth factor (VEGF) in the carcinogenesis of nickel. Methods Human embryonic lung fibroblasts (WI-38) were treated with Ni2O3 for 24, 48 and 72 h, respectively. The mRNA expression of TRX, HIF-1 and VEGF was detected by RT-PCR. Results After treated with Ni2O3 for 24 h, the mRNA expression of VEGF in each concentration group (5, 10 and 15 μg / ml) was significantly higher than that in the control group [(0.76 ± 0.04), (0.78 ± 0.06) and (0.69 ± 0.01) (0.58 ± 0.02) than the control group (P <0.05). 48 and 72 h treatment results also increased compared with the control group. Compared with the control group (1.06 ± 0.09), the mRNA expression of TRX (0.36 ± 0.15), (0.31 ± 0.07) and (0.31 ± 0.02) in each concentration group decreased after 72 h of Ni2O3 treatment (P <0.05). The mRNA expression of HIF-1 in 5 and 10μg / ml Ni2O3 group was significantly higher than that in the control group 〔(1.01 ± 0.04) and (0.82 ± 0.12〕〕 48h after treatment ([0.47 ± 0.02], P <0.05] (0.66 ± 0.10) and (0.69 ± 0.13) respectively after 72 h. There was no significant difference between the control group and the 15 μg / ml Ni 2 O 3 group (24, 48 and 72 h after treatment). Conclusion The changes of gene expression related to oxidative damage such as TRX, HIF-1 and VEGF may play an important role in nickel-induced cell transformation.