丹皮酚对表柔比星诱导的膀胱癌BIU-87细胞凋亡的影响及机制研究

Effect of paeonol on BIU-87 cell apoptosis induced by epirubicin and its mechanism

目的:探讨丹皮酚对表柔比星诱导的膀胱癌BIU-87细胞凋亡的影响,并对其及作用的分子机制进行探讨。方法:将培养的人膀胱癌BIU-87细胞以不同浓度的丹皮酚处理后,采用MTT法检测对细胞增殖抑制的影响,流式细胞术检测细胞凋亡情况,酶联免疫吸附测定法(ELISA)检测白细胞介素-1β(IL-1β)水平,Western blot检测细胞中活化的含半胱氨酸的天冬氨酸蛋白水解酶3(Cleaved Caspase-3)和生存素(survivin)的表达水平。结果:丹皮酚抑制人膀胱癌细胞BIU-87增殖。表柔比星抑制膀胱癌细胞BIU-87的增殖,诱导细胞凋亡,促进Cleaved Caspase-3、IL-1β的表达,抑制survivin的表达,与对照组比较,差异具有统计学意义(P<0.05)。丹皮酚可增强表柔比星对膀胱癌细胞BIU-87增殖抑制作用,增强表柔比星对细胞凋亡的诱导,与EPI组及对照组比较,差异具有统计学意义(P<0.05)。结论:丹皮酚可增强表柔比星诱导膀胱癌细胞的凋亡和增殖抑制作用,其作用机制与Caspase-3的活化,下调survivin的表达,促进IL-1β的分泌有关。

Objective:To explore the effect of paeonol on epirubicin-induced BIU-87 cell apoptosis induced by epirubicin,and to explore the molecular mechanism of its action.Methods:The cultured human bladder cancer BIU-87 cells were treated with paeonol at different concentrations.MTT assay was used to examine the effect of cell proliferation inhibition.Flow cytometry was used to detect apoptosis,and enzyme-linked immunosorbent assay(ELISA)was used to detect secretion.Interleukin-1β(IL-1β)levels were detected by Western blotting to detect the expression of activated cysteine-containing caspase-3 and survivin.Results:Paeonol inhibited the proliferation of human bladder cancer cell line BIU-87.Epirubicin inhibited the proliferation of bladder cancer cell line BIU-87,induced apoptosis,promoted the expression of Cleaved Caspase-3 and IL-1β,and inhibited the expression of survivin.The difference was statistically significant(P<0.05).Paeonol can enhance the inhibitory effect of epirubicin on the proliferation of bladder cancer cell line BIU-87 and enhance the induction of apoptosis by epirubicin.Compared with the epirubicin group and the control group,the difference was statistically significant(P<0.05).Conclusion:Paeonol can enhance the apoptosis rate and proliferation inhibition of bladder cancer cells induced by epirubicin.Its mechanism of action is related to the activation of Caspase-3,down-regulation of survivin expression,and promotion of IL-1βsecretion.