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目的:本研究旨在探讨地西他滨联合紫杉醇对紫杉醇耐药细胞MCF-7的细胞增殖抑制和诱导凋亡作用的影响。方法:采用CCK-8方法检测联合用药(地西他滨+紫杉醇)或单独用药(地西他滨、紫杉醇)组不同给药浓度在24,48,72 h对耐药细胞的增殖抑制作用,流式细胞仪检测不同给药组给药后48 h的细胞凋亡率。结果:CCK-8结果显示联合用药组相较于单药组对细胞增殖抑制作用显著增加(P<0.05),呈剂量依赖性,不同给药组的细胞增殖抑制率随着时间延长而增大;诱导细胞凋亡结果显示,48 h地西他滨单药组和紫杉醇单药组的细胞凋亡率分别是(20.4±1.98)%和(21.8±3.34)%,联合用药组的细胞凋亡率增加至(70.8±8.23)%。结论:地西他滨联合紫杉醇对紫杉醇耐药MCF-7细胞株的增殖抑制作用增加,促进耐药细胞的凋亡,地西他滨联合紫杉醇对耐药细胞株具有协同抗肿瘤作用。
Aims: This study was designed to investigate the effect of decitabine combined with paclitaxel on paclitaxel-resistant cells MCF-7 cell proliferation and apoptosis induced by apoptosis. Methods: The proliferation inhibition of drug-resistant cells was detected by CCK-8 assay at 24,48 and 72 h in combination with drugs (decitabine + paclitaxel) or alone (decitabine, paclitaxel) Flow cytometry was used to detect the apoptotic rate at 48 h after administration in different groups. Results: The results of CCK-8 showed that compared with the monotherapy group, the inhibitory effect of CCK-8 on cell proliferation was significantly increased (P <0.05) in a dose-dependent manner. The inhibition rate of cell proliferation in different groups increased with time . The results of apoptosis showed that the apoptotic rate in the 48 h decitabine monotherapy group and the paclitaxel monotherapy group were (20.4 ± 1.98)% and (21.8 ± 3.34)%, respectively, and the apoptosis rate The rate increased to (70.8 ± 8.23)%. CONCLUSION: Decitabine plus paclitaxel can increase the proliferation of paclitaxel-resistant MCF-7 cells and promote the apoptosis of drug-resistant cells. Decitabine combined with paclitaxel has a synergistic anti-tumor effect on drug-resistant cell lines.