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目的研究砷剂联合抗坏血酸协同诱导多发性骨髓瘤细胞株凋亡的机制。方法将培养的MM细胞株KM3分为:①对照组;②ATO单药组;③ATO+AA组;④AA单药组;⑤ATO+α生育酚组;⑥α生育酚单药组。分别检测细胞活力、细胞凋亡率、线粒体膜电位和细胞内GSH、H2O2水平。结果①ATO诱导MM细胞凋亡,AA增强其作用,α生育酚减弱其作用;②AA降低细胞内GSH水平,α生育酚升高细胞内GSH;③AA和α生育酚均升高细胞内H2O2水平;④ATO降低细胞线粒体膜电位,AA增强ATO的作用,α生育酚减弱其作用。结论砷剂诱导肿瘤细胞凋亡敏感性与细胞内GSH水平呈负相关,砷剂通过降低细胞线粒体膜电位,诱导细胞凋亡。AA通过降低细胞内的GSH水平,增加细胞对砷剂的敏感性。选择其他的还原剂无此作用。
Objective To study the mechanism of arsenic combined with ascorbic acid inducing apoptosis of multiple myeloma cell lines. Methods The cultured KM cell line KM3 was divided into: ① control group; ② ATO single drug group; ③ ATO + AA group; ④ AA single drug group; ⑤ ATO + α tocopherol group; ⑥ α tocopherol single drug group. Cell viability, apoptosis rate, mitochondrial membrane potential and intracellular GSH, H2O2 levels were measured. Results ①ATO induced the apoptosis of MM cells. AA enhanced its action and α-tocopherol attenuated its action; ②AA reduced the level of intracellular GSH, α-tocopherol increased intracellular GSH; ③AA and α-tocopherol increased intracellular H2O2 levels; Reduce mitochondrial membrane potential, AA enhance the role of ATO, α-tocopherol weakens its role. Conclusion The sensitivity of arsenic-induced tumor cell apoptosis is negatively correlated with the level of intracellular GSH. Arsenic trioxide can induce cell apoptosis by decreasing mitochondrial membrane potential. AA increases the sensitivity of cells to arsenic agents by reducing intracellular levels of GSH. Choose other reducing agent without this effect.