芍药苷对肺腺癌细胞A549凋亡的诱导作用

Induction Effect of Paeoniflorin on the Apoptosis of Lung Adenocarcinoma A549 Cells

目的：研究芍药苷对肺腺癌A549细胞凋亡的诱导作用。方法：以0（阴性对照）、5、10、20、40μmol/L芍药苷培养A549细胞48 h后,以MTT法检测A549细胞活力。上述浓度芍药苷培养A549细胞24 h后,酶标法检测半胱氨酸天冬氨酸蛋白水解酶3（Caspase-3）活性;Western blot法检测Bcl-xl、Bax、核因子κB p65（NF-κB p65）、磷酸化核因子κB p65（NF-κB pp65）蛋白表达。结果：与阴性对照比较,5~40μmol/L芍药苷培养A549细胞48 h后,细胞活力减弱;5~40μmol/L芍药苷培养细胞24 h后,细胞Caspase-3活性、Bax蛋白表达增强;10~40μmol/L芍药苷培养细胞24 h后,细胞Bcl-xl蛋白表达减弱,NF-κB pp65蛋白表达减弱;以上差异均具有统计学意义（P〈0.01或P〈0.05）。结论：芍药苷可诱导A549细胞凋亡,其机制可能与激活NF-κB信号通路、调节相关基因表达有关。

OBJECTIVE：To study the induction effect of paeoniflorin on the apoptosis of lung adenocarcinoma A549 cells.METHODS：MTT method was used to detect the viability of A549 cells 48 h after the cells were cultured with paeoniflorin of 0（negative control）,5,10,20 and 40 μmol/L.24 h after A549 cells were cultured with paeoniflorin at the above-mentioned concentrations,enzyme-linked immunosorbent assay was employed to detect the viability of cysteinyl aspartate specific proteinase 3（Caspase-3）,and Western blot to determine the protein expression of Bcl-xl,Bax,nuclear factor κB p65（NF-κB p65）and phosphorylated nuclear factor κB p65（NF-κB pp65）.RESULTS：Compared to the negative control group,A549 cells cultured with paeoniflorin of 5-40 μmol/L for 48 h showed lower cell viability;A549 cell cultured with paeoniflorin of 5-40 μmol/L for 24 h showed higher activity of Caspase-3 and the expression of Bax;A549 cell cultured with paeoniflorin of 10-40 μ mol/L for 24 h showed lower protein expression of Bcl-xl and NF-κB pp65.There were statistically difference（P〈0.01 or P〈0.05）.CONCLUSIONS：Paeoniflorin induces the apoptosis of A549 cells by a mechanism which may be related to the activation of NF-κB signaling pathway and regulation related gene expression.