摘要
【目的】探讨芍药苷对黑色素瘤 A‐375细胞凋亡的影响。【方法】采用不同浓度(0.5、1、2 mg/mL)芍药苷处理黑色素瘤 A‐375细胞后继续培养24 h ,MTT 法检测细胞抑制率,Hoechst 染色检测细胞形态, Western Blot 检测抑癌基因 Bax 、细胞增殖抗原(PCNA)、核因子κB(NF‐κB) p65蛋白表达。【结果】随着给药浓度的增加,芍药苷对 A‐375细胞的抑制率逐渐增高,在48 h 达到高峰;Hoechst 染色结果表明随着浓度的逐渐增高,细胞裂解强度增大;Western Blot 结果表明芍药苷上调 Bax 表达,下调 PCNA 表达,抑制 NF‐κB p65表达,且呈剂量依赖性。【结论】芍药苷诱导黑色素瘤 A‐375细胞凋亡,可能是通过 NF‐κB 信号通路发挥作用。
[Objective] To explore the apoptotic effects and mechanism of paeoniflorin in melanoma cell A‐375 .[Methods] Melanoma cell A‐375 was treated with paeoniflorin (0 .5 ,1 ,2 mg/mL) .The cell apoptotic rate was detected by methyl thiazolyl tetrazolium (MTT ) assay .Cellular morphology was examined by Ho‐echst staining .The expressions of Bax ,PCNA and NFκB p65 were assessed by Western blot .[Results] M TT assay demonstrated paeoniflorin (0 .5 ,1 ,2 mg /mL) could reduced cell viability .And inhibitory effect peaked at 48h .Hoechst staining indicated that paeoniflorin could induce cell apoptosis in a dose‐dependent way .And paeoniflorin could down‐regulate the expressions of PCNA and NFκB p65 and up‐regulate the expression of Bax in a concentration‐dependent way .[Conclusion] Paeoniflorin induces apoptosis through a NF‐κB signal pathway in melanoma cell A‐375 .
出处
《医学临床研究》
CAS
2015年第6期1162-1164,共3页
Journal of Clinical Research