目的 探讨芍药苷对人恶性黑色素瘤细胞A375增殖的体外抑制作用及其作用机制。方法 不同浓度芍药苷(3、10、30 μmol/L)作用于黑色素瘤细胞A375,MTT法检测细胞活力,流式细胞术检测细胞周期情况,Western blotting法检测NFκB p65信号通路激活情况及下游靶分子Bax、Bcl-2、Cyclin D1、Cyclin E的表达。结果 与对照组比较,随着给药浓度的增加,芍药苷对黑色素瘤细胞A375抑制作用逐渐增强,30 μmol/L作用48 h时抑制作用最高,并使A375细胞周期阻滞在G1期;芍药苷显著抑制NFκB p65、IκBα的磷酸化,下调Bcl-2、Cyclin D1、Cyclin E的表达,上调Bax表达,差异均具有统计学意义(P < 0.01)。结论 芍药苷能抑制人黑色素瘤细胞A375体外增殖,可能是通过NF-κB信号通路发挥作用的。

Objective To study inhibitory action of paeoniflorin on human malignant melanoma cell A375 in vitro and explored its mechanism. Methods A375 cells were treated with paeoniflorin (3, 10, and 30 μmol/L). The viability of the cell was detected by MTT assay. Cell cycle change was detected by flow cytometry. The activition of NFκB p65 signaling pathway and expression of Bax, Bcl-2, Cyclin D1, and Cyclin E were assessed by Western blotting method. Results Compared with control group, paeoniflorin (3, 10, and 30 μmol/L) could reduce cell viability, the inhibitory effect was highest in 48 h at concentration of 30 μmol/L. Moreover, paeoniflorin could make A375 cell arrest in G1 phase. Western blotting assays presented paeoniflorin could suppress the phosphorylation of NFκB p65 and IκBα, down-regulate the expression of Bcl-2, and up-regulate the expression of Bax, Cyclin D1, and Cyclin E with significant differences (P < 0.01). Conclusion Paeoniflorin has inhibitory action on the proliferation of human malignant melanoma cell A375 in vitro, which may be related to NF-κB signal pathway.