精品文档---下载后可任意编辑硼替佐米对白血病耐药细胞 K562/A02 化疗增敏效应讨论的开题报告【摘要】：目的：探究硼替佐米对白血病耐药细胞 K562/A02 的化疗增敏效应和机制。方法：采纳 MTT 法检测硼替佐米和化疗药物阿霉素对 K562/A02 细胞的增殖抑制作用；采纳流式细胞术检测硼替佐米和阿霉素联合应用后 K562/A02 细胞凋亡率和细胞周期的变化；用 Western blotting 技术检测硼替佐米对 K562/A02 细胞内 Bcl-2 家族蛋白的表达变化。结果：硼替佐米和阿霉素单药对 K562/A02 细胞均有抑制作用，硼替佐米对 K562/A02 细胞的半数抑制浓度（IC50）为 0.68 μM，阿霉素的 IC50 为 0.02 μM；硼替佐米与阿霉素联合应用后可显著提高K562/A02 细胞凋亡率和 G0/G1 期细胞比例，同时抑制 S 期细胞比例；硼替佐米可下调 K562/A02 细胞内 Bcl-2、Bcl-xl、Mcl-1 等抗凋亡蛋白的表达。结论：硼替佐米能够显著增强化疗药物阿霉素对 K562/A02 细胞的化疗增敏效应，可能是通过下调 Bcl-2 家族蛋白的表达，促进肿瘤细胞凋亡的机制实现的。【关键词】：硼替佐米；K562/A02 细胞；阿霉素；化疗增敏；Bcl-2 家族蛋白【Abstract】: Objective: To explore the chemosensitization effect and mechanism of bortezomib on drug-resistant leukemia cells K562/A02. Methods: MTT assay was used to detect the growth inhibitory effect of bortezomib and chemotherapy drug idarubicin on K562/A02 cells; flow cytometry was used to detect the changes of apoptosis rate and cell cycle of K562/A02 cells after treatment with bortezomib and idarubicin in combination; western blotting was used to detect the expression changes of Bcl-2 family proteins in K562/A02 cells after treatment with bortezomib. Results: Bortezomib and idarubicin alone showed inhibitory effect on K562/A02 cells, with IC50 of 0.68 μM and 0.02 μM, respectively; after the combination of bortezomib and idarubicin, the apoptosis rate and G0/G1 cell ratio of K562/A02 cells were significantly increased while the S phase cell ratio was inhibited; bortezomib down-regulated the expression of anti-apoptotic proteins such as Bcl-2, Bcl-xl and Mcl-1 in K562/A02 cells. Conclusion: Bortezomib can significantly enhance the chemosensitization effect of idarubicin on K562/A02 cells, which may be achieved by down-regulating the 精品文档---下载后可任意编辑expression of Bcl-2 family proteins and promoting the mechanism of tumor cell apoptosis.【Keywords】: bortezomib; K562/A02 cells; idarubicin; chemosensitization; Bcl-2 family proteins
