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目的探讨粉防己碱逆转ＭＤＲ细胞凋亡抗性的作用及其机制。方法ＭＤＲ细胞株ＭＣＦ－７／Ａｄｒ与其相应的敏感株ＭＣＦ－７进行对比研究。比较粉防己碱对阿霉素（Ｄｏｘ）诱导ＭＤＲ细胞及其相应的敏感株的凋亡作用。并比较粉防己碱对ＭＤＲ细胞及其相应的敏感株的细胞ｂｃｌ－２蛋白的表达的影响。细胞凋亡及ｂｃｌ－２蛋白表达的测定以流式细胞仪法。结果加入Ｄｏｘ共同培养２４ｈ可诱导７４．６％ＭＣＦ－７细胞凋亡，而只引起１４．３％的ＭＣＦ－７／Ａｄｒ细胞凋亡。只加入粉防己碱共同培养２４ｈ，未见明显增加ＭＤＲ细胞及其相应敏感细胞的凋亡百分比。Ｄｏｘ＋粉防己碱能显著地使ＭＤＲ细胞的凋亡增至４７．０％，与单独用Ｄｏｘ组相比较，差异有显著性（Ｐ＜０．０１），而敏感细胞株为７７．８％，与单独用Ｄｏｘ组相比较，差异无显著性（Ｐ＞０．０５）。ＭＤＲ细胞株与其相应的敏感株ｂｃｌ－２蛋白表达水平均较低且差异无显著性。加入粉防己碱对ＭＤＲ细胞株与其相应的敏感株ｂｃｌ－２蛋白表达水平均未见明显影响。结论粉防己碱能逆转ＭＤＲ细胞对Ｄｏｘ的凋亡抗性。其逆转机制可能与ｂｃｌ－２蛋白表达无关。粉防己碱逆转ＭＤＲ细胞ＭＣＲ－７／ＡＤＲ对Ｄｏｘ的凋亡抗性的机制有待进?
Objective To investigate the effect of tetrandrine on MDR cell apoptosis and its mechanism. Methods MDR cell line MCF-7 / Adr and its corresponding sensitive strain MCF-7 were compared. To compare the apoptotic effect of tetrandrine on doxorubicin (Dox) -induced MDR cells and their corresponding sensitive strains. And compare the effect of tetrandrine on the expression of bcl-2 protein in MDR cells and their corresponding sensitive strains. Apoptosis and bcl-2 protein expression were measured by flow cytometry. Results Incubation with Dox for 24 h induces apoptosis in 74.6% MCF-7 cells and only induces apoptosis in 14.3% of MCF-7 / Adr cells. Only adding tetrandrine for 24h co-cultured, no significant increase in MDR cells and their corresponding sensitive cells apoptosis percentage. Dox + Tetrandrine significantly increased the apoptosis rate of MDR cells to 47.0%, which was significantly different from that of Dox group (P <0.01), while the sensitive cell strain was 77.8% Compared with the Dox group alone, the difference was not significant (P> 0.05). The expression of bcl-2 protein in MDR cell lines and their corresponding sensitive strains was low and the difference was insignificant. Addition of tetrandrine had no significant effect on the expression of bcl-2 protein in MDR cell lines and their corresponding sensitive strains. Conclusion Tetrandrine can reverse the apoptosis resistance of MDR cells to Dox. The reversal mechanism may not be related to bcl-2 protein expression. Tetrandrine reverses MDR cells MCR-7 / ADR Dox apoptosis resistance mechanisms to be?