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目的探讨甲醛对HepG2细胞凋亡的影响。方法以0.004、0.02、0.1、0.5、2.5、12.5 mmol/L的甲醛(formaldehyde)分别处理人肝癌HepG2细胞24和48 h,采用MTT法检测细胞活性。分别以0.004、0.02、0.1 mmol/L的甲醛处理人肝癌HepG2细胞24和48 h,采用Western blot法检测p53、mdm2、Caspase-3、RIP1、RIP3和NF-κB的蛋白表达水平。结果与阴性对照组相比较,0.5~12.5 mmol/L FA染毒24和48 h可显著降低HepG2细胞活性(P<0.05);染毒24 h后Caspase-3蛋白表达降低(P<0.05);p53、p-p53、mdm2、RIP3表达水平在染毒24和48 h后均明显降低(P<0.05);cleaved RIP1表达水平在0.1 mmol/L剂量染毒24和48 h后表达增加(P<0.05)上述变化均有统计学意义;染毒24和48 h后NF-κB蛋白表达无明显变化。结论甲醛可能是通过死亡受体途径而不是线粒体途径引起肝细胞凋亡。
Objective To investigate the effect of formaldehyde on the apoptosis of HepG2 cells. Methods HepG2 cells were treated with 0.004, 0.02, 0.1, 0.5, 2.5 and 12.5 mmol / L of formaldehyde for 24 and 48 h respectively. The cell viability was measured by MTT assay. The expression of p53, mdm2, Caspase-3, RIP1, RIP3 and NF-κB protein in HepG2 cells were detected by Western blot at 0.004, 0.02, 0.1 mmol / L formaldehyde for 24 and 48 h, respectively. Results Compared with the negative control group, the activities of HepG2 cells in 0.5 ~ 12.5 mmol / L FA treatment for 24 and 48 h were significantly decreased (P <0.05), while the expression of Caspase - 3 protein was decreased in 24 h (P <0.05). The expression of cleaved RIP1 was significantly decreased at 24 and 48 h (P <0.05), while the expression of cleaved RIP1 was increased at 24 and 48 h (P < 0.05) The above changes were statistically significant; at 24 and 48 h after exposure, the expression of NF-κB protein had no significant change. Conclusion Formaldehyde may induce hepatocyte apoptosis through the death receptor pathway rather than the mitochondrial pathway.