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目的探讨氯乙烯(VCM)对细胞周期G1/S关卡功能影响及可能的机制。方法将人正常肝细胞HL-7702暴露于VCM气体(体积分数为0.8%、2.5%、7.5%、15.0%和30.0%)和空气(对照组)48 h后用流式细胞仪检测HL-7702细胞周期;Western blot测定细胞中G1/S关卡相关蛋白表达水平。结果染毒48 h后,在<7.5%剂量时,HL-7702细胞G0/G1期细胞百分数随染毒剂量增加呈上升趋势,与对照组[(73.35±1.56)%]比较,7.5%剂量组G0/G1期细胞百分比[(78.52±4.46)%]升高,差异有统计学意义(P<0.01);与对照组[(12.85±0.02)%]比较,2.5%剂量组S期细胞百分比[(10.97±0.17)%]下降,差异有统计学意义(P<0.05);细胞周期蛋白依赖性激酶(CDK 4)和P16蛋白表达量均呈上升趋势,与对照组比较,7.5%剂量组HL-7702细胞CDK 4、P16表达[分别为(1.43±0.51)、(0.80±0.30)]均升高,差异均有统计学意义(均P<0.05)。结论低剂量VCM染毒可使肝细胞发生G1期阻滞,高剂量时G1期阻滞作用消失;其机制主要与上调P16、CDK 4蛋白表达有关。
Objective To investigate the effect of VCM on cell cycle G1 / S and its possible mechanism. Methods HL-7702 cells were exposed to VCM gas (0.8%, 2.5%, 7.5%, 15.0% and 30.0%, respectively) and air (control group) Cell cycle; Western blot determination of G1 / S level of cell-related protein expression levels. Results At 48 hours after exposure, the percentage of cells in G0 / G1 phase of HL-7702 cells increased with the dose of 7.5%, compared with the control group [(73.35 ± 1.56)%], 7.5% Compared with the control group [(12.85 ± 0.02)%], the percentage of S phase cells in the 2.5% dose group was significantly higher than that in the control group [(78.52 ± 4.46)%] in the G0 / (10.97 ± 0.17)%], the difference was statistically significant (P <0.05); the expression of CDK 4 and P16 protein showed an upward trend, compared with the control group, 7.5% dose group HL The expressions of CDK 4 and P16 in -7702 cells were significantly higher than those in control group (1.43 ± 0.51 and 0.80 ± 0.30, respectively) (all P <0.05). Conclusion Low dose VCM can induce G1 phase arrest in hepatocytes and disappear in G1 phase when treated with high dose of VCM. The mechanism is mainly related to up-regulation of P16 and CDK4 protein expression.