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目的 观察抗癌新药 2 0 (R) 人参皂甙Rg3(2 0 (R) ginsenoside ,Rg3)对K5 6 2 /ADM多耐药细胞株逆转MDR机制。方法 应用MTT法确定ADM和Rg3的细胞毒 ;用荧光分光光度仪测定K5 6 2 /ADM细胞内阿霉素 (Adriamycin ,ADM )的浓度 ;流式细胞仪检测细胞凋亡率和表达P 170糖蛋白 (P glycoprotein ,Pgp)的K5 6 2 /ADM的细胞含量。 结果 (1)K5 6 2 /ADM细胞对阿霉素 (Adriamycin ,ADM )的抗性比K5 6 2细胞高 11倍 ,但两者对Rg3的IC50 分别为 11 76± 0 33μg/ml、10 4 9± 0 30 μg/ml,无显著性差异 (P >0 0 5 )。(2 )无毒剂量和低毒剂量的Rg3能显著提高K5 6 2 /ADM细胞内ADM的浓度 ,使该细胞对ADM的敏感性明显提高。 (3)Rg3对K5 6 2 /ADM细胞有较强的抑制生长和诱导凋亡作用 ,并有时间和浓度依赖性。(4)Rg3对表达P 170糖蛋白的K5 6 2 /ADM细胞的百分含量无显著性影响。结论 2 0 (R) 人参皂甙Rg3不仅是抑制肿瘤生长和转移的抗瘤剂 ,也是一种有效的MDR逆转剂和细胞凋亡诱导剂
Objective To observe the mechanism of reversal of MDR in multidrug-resistant K5 6 2 /ADM cell line by 20 (R) ginsenoside Rg3 (20 s ginsenoside, Rg3). Methods The cytotoxicity of ADM and Rg3 was determined by MTT assay; the concentration of Adriamycin (ADM) in K562/ADM cells was measured by fluorescence spectrophotometer; the apoptosis rate and the expression of P 170 sugar were detected by flow cytometry. Protein Content of Protein (P glycoprotein, Pgp) K5 6 2 /ADM Results (1) K562/ADM cells were 11 times more resistant to Adriamycin (ADM) than K562 cells, but their IC50 for Rg3 was 1176±0 33 μg/ml, 10 4 respectively. 9± 0 30 μg/ml, no significant difference (P > 0 05). (2) The non-toxic dose and low toxic dose of Rg3 can significantly increase the concentration of ADM in K562/ADM cells, so that the sensitivity of the cells to ADM is significantly improved. (3) Rg3 inhibited the growth and induced apoptosis of K562/ADM cells in a time- and concentration-dependent manner. (4) Rg3 had no significant effect on the percentage of K562/ADM cells expressing P170 glycoprotein. Conclusion 20 (R) ginsenoside Rg3 is not only an antitumor agent that inhibits tumor growth and metastasis, but also an effective MDR reversal agent and inducer of apoptosis.