芍药苷对HepG2肝癌细胞凋亡的诱导作用

目的:探讨芍药苷(Paeoniflorin)对HepG2肝癌细胞凋亡的诱导作用,并考察其作用机制。方法:用不同浓度芍药苷(0.5,2mg/mL)对HepG2肝癌细胞进行培养,采用MTT法检测细胞活力,酶标法检测Caspase 3活性,western blot法检测NF-κB信号通路相关蛋白表达。结果:随着给药浓度的增加,芍药苷能逐渐降低HepG2肝癌细胞活力,在48小时抑制率最高;并能提高Caspase 3活性,抑制细胞核内NF-κB p65磷酸化,IκBα磷酸化,从而促进细胞凋亡。结论:芍药苷可能通过NF-κB信号通路诱导HepG2肝癌细胞凋亡,达到抗肿瘤效果。

Apoptotic Induction Effects of Paeoniflorin on Hepatoma Carcinoma Cells

Objective: To explore apoptotic induction effects of paeoniflorin on hepatoma carcinoma cells (HepG2), and to investigate its mechanism. Methods: HepG2 cells were cultivated with different concentrations of paeoniflorin (0.5, 2 mg/mL), cell viability was detected by MTT method, Caspase 3 activity measured by enzyme linked immunosorbent assay and the expression of NF-κB signaling pathway related protein by western blot method. Results: As the concentrations of the drug increased, paeoniflorin could decrease the viability of HepG2 cells gradu-ally, and the inhibition rate reached the highest within 48 hours; it increased Caspase 3 activity, inhibited the phos-phorylation of NF-κB p65 and IκBα, thereby to promote cellular apoptosis. Conclusion: Paeoniflorin could obtain anti-tumor effects by inducing the apoptosis of HepG2 cells via NF-κB signaling pathway.