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目的体外观察硒酸酯多糖(KSC)与紫杉醇(Taxol)对肝癌细胞HepG-2生长的协同抑制效应,并探讨其作用机制。方法 MTT法观察KSC和Taxol单用及合用对HepG-2细胞的抑制作用,并计算两药合用72 h的IC50及合用指数CDI;采用荧光显微镜、流式细胞仪观察上述药物作用后HepG-2细胞形态学、细胞周期及凋亡率的改变。结果MTT结果显示,KSC与Taxol均能显著抑制HepG-2细胞的增殖,且具有时效-量效关系,联合组效果优于单一用药组;KSC、Taxol单用72 h的IC50分别为46.632 mg.L-1和1.684 nmol.L-1,两药联合应用后的IC50分别降至31.684 mg.L-1和0.272 nmol.L-1。30 mg.L-1的KSC与0.5~5 nmol.L-1的Taxol联合效果表现为协同作用(CDI<1.0)。细胞形态学观察可见细胞数减少,细胞核明显变小,并可见致密强荧光及凋亡小体。流式细胞术结果显示两药均作用于S期,联合组既可发生S期周期阻滞,又可诱导凋亡,但凋亡率低于Taxol单独组。结论 KSC与化疗药物Taxol联合可产生协同作用,诱导肿瘤细胞周期阻滞可能为其主要的抗肿瘤机制之一。
Objective To observe the synergistic inhibitory effect of KSC and Taxol on the growth of HepG-2 cells in vitro and to explore its mechanism. Methods MTT method was used to observe the inhibitory effect of KSC and Taxol alone or in combination on HepG-2 cells. The IC50 of 72 hours and the combined index of CDI were calculated. The expression of HepG-2 was observed by fluorescence microscope and flow cytometry Cell morphology, cell cycle and apoptosis rate changes. Results MTT assay showed that both KSC and Taxol could significantly inhibit the proliferation of HepG-2 cells, and had an effect of time-dose-effect. The combination group was better than single drug group. The IC50 of KSC and Taxol alone for 72 h was 46.632 mg. L-1 and 1.684 nmol.L-1, the IC50 of the combination of the two drugs decreased to 31.684 mg.L-1 and 0.272 nmol.L-1.30 mg.L-1 KSC and 0.5 ~ 5 nmol.L -1 synergistic effects of Taxol showed synergism (CDI <1.0). Cell morphological observation showed that the number of cells decreased, the nucleus was significantly smaller, and visible dense fluorescence and apoptotic bodies. Flow cytometry results show that both drugs act on the S phase, the combination group can occur S cycle arrest, but also induce apoptosis, but the apoptotic rate was lower than the Taxol alone group. Conclusion Combination of KSC with Taxol can produce synergistic effect and induce tumor cell cycle arrest may be one of its main anti-tumor mechanisms.