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目的:观察雷公藤内酯醇与紫杉醇联合用药对人乳腺癌MCF-7细胞是否有协同效应,并初步探讨其作用机制。方法:将对数生长期细胞随机分为4组,分别为雷公藤内酯醇单药组、紫杉醇单药组、两药联合组和正常对照组。MTT比色法检测各组细胞的生长抑制率;流式细胞术检测各组细胞凋亡和周期;Western blot法检测各组ERα蛋白的表达。结果:雷公藤内酯醇在较低配比下与紫杉醇联合有强协同抑制作用;联合组细胞凋亡率明显高于单药组(P<0.05);雷公藤内酯醇组S期细胞比例明显增加,紫杉醇组与联合组G2/M期的细胞比例明显增高(P<0.05);雷公藤内酯醇和联合组均能较紫杉醇组更明显下调ERα蛋白表达。结论:雷公藤内酯醇在低剂量配比下与紫杉醇联合,对人乳腺癌MCF-7细胞有强协同抑制作用。协同抑制作用机制可能与阻断雌激素信号通路有关。
Objective: To observe whether triptolide combined with paclitaxel has a synergistic effect on human breast cancer MCF-7 cells and to explore its mechanism. Methods: The logarithmic growth phase cells were randomly divided into 4 groups, namely triptolide single group, paclitaxel single group, two drug combination group and normal control group. MTT assay was used to detect the growth inhibition rate of each group. Flow cytometry was used to detect the apoptosis and cycle of each group. The expression of ERα protein in each group was detected by Western blot. Results: Triptolide had a synergistic inhibitory effect in combination with paclitaxel at a lower dose. The apoptosis rate in the combination group was significantly higher than that in the single drug group (P <0.05). The proportion of cells in the triptolide group was significantly increased , And the proportion of cells in G2 / M phase of paclitaxel group and combination group was significantly higher than that of paclitaxel group (P <0.05). Both triptolide and combination group could downregulate ERα protein expression more significantly than paclitaxel group. Conclusion: Triptolide combined with paclitaxel at a low dose ratio has a strong synergistic inhibitory effect on human breast cancer MCF-7 cells. Synergistic inhibition mechanism may be related to blocking the estrogen signaling pathway.