目的 探討芍藥苷對人惡性黑色素瘤細(xì)胞A375增殖的體外抑制作用及其作用機制。方法 不同濃度芍藥苷(3、10、30 μmol/L)作用于黑色素瘤細(xì)胞A375,MTT法檢測細(xì)胞活力,流式細(xì)胞術(shù)檢測細(xì)胞周期情況,Western blotting法檢測NFκB p65信號通路激活情況及下游靶分子Bax、Bcl-2、Cyclin D1、Cyclin E的表達(dá)。結(jié)果 與對照組比較,隨著給藥濃度的增加,芍藥苷對黑色素瘤細(xì)胞A375抑制作用逐漸增強,30 μmol/L作用48 h時抑制作用最高,并使A375細(xì)胞周期阻滯在G1期;芍藥苷顯著抑制NFκB p65、IκBα的磷酸化,下調(diào)Bcl-2、Cyclin D1、Cyclin E的表達(dá),上調(diào)Bax表達(dá),差異均具有統(tǒng)計學(xué)意義(P < 0.01)。結(jié)論 芍藥苷能抑制人黑色素瘤細(xì)胞A375體外增殖,可能是通過NF-κB信號通路發(fā)揮作用的。

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.