大黄素对人卵巢癌紫杉醇耐药细胞株SKOV3/TAX耐药的逆转作用

The reversal effect of emodin on human ovarian cancer SKOV3/TAX cells drug-resistant to taxol

目的研究大黄素(emodin)体外逆转人卵巢癌紫杉醇耐药细胞株SKOV3/TAX的紫杉醇耐药效应,探讨其可能机制。方法采用四甲基偶氮唑蓝(MTT)法检测大黄素对SKOV3/TAX的细胞毒作用,测定非毒性剂量大黄素联合紫杉醇作用后,SKOV3/TAX对紫杉醇耐药性的变化,采用克隆形成实验检测大黄素与紫杉醇联用时,细胞克隆形成能力。采用流式细胞技术(FCM)检测细胞凋亡情况。结果不同浓度大黄素对紫杉醇耐药细胞SKOV3/TAX有剂量和时间依赖性的抑制作用。选用对细胞抑制率较低浓度的大黄素与紫杉醇联合使用,使紫杉醇对其耐药细胞SKOV3/TAX细胞的IC50明显下降,且逆转倍数随作用时间而延长而增大。大黄素能抑制细胞的克隆形成能力,当大黄素与紫杉醇联用时,大黄素增加紫杉醇对SKOV3/TAX细胞的增殖抑制作用。大黄素在抑制细胞增殖的同时,尚可诱导细胞凋亡,且大黄素与紫杉醇联和用药后诱导细胞凋亡作用更强,大黄素能增加紫杉醇的细胞凋亡指数。结论大黄素可以逆转紫杉醇引发的卵巢癌耐药,抑制细胞增殖,促进细胞凋亡。

Objective To study the reversal effect of emodin on human ovarian taxol-resistant cancer cell SKOV3/TAX and to explore the possible mechanism. Methods The cell viability and colony formation were detected by MTT assay and colony formation assay respectively,apoptosis was detected by flow cytometry. Results The dosedependent and time-dependent inhibition effect of emodin was found on SKOV3/TAX cells. Emodin and paclitaxel comibined treatment of SKOV3/TAX reversed the drug-resistance of Taxol to SKOV3/TAX cells. Emodin and taxol inhibited the proliferation of SKOV3/TAX cells. Emodin can inhibit cell proliferation by inducing apoptosis, and the combination of emodin and taxol increased the apoptosis rate of SKOV3/TAX cells. Conclusion Drug resistance induced by paclitaxel can be reversed by emodin in ovarian cancer, the possible mechanism is the inhibition of cell proliferation and the promotion of cell apoptosis.