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研究盐酸千金藤碱(cepharanthine hydrochloride,CH)逆转K562/ADR细胞多药耐药性及其机制。采用MTT法检测多柔比星(adriamycin,ADR)单用及分别与CH、维拉帕米(verapamil,VER)合用的细胞毒作用;采用流式细胞仪,测定CH对细胞内ADR蓄积、罗丹明123(Rho123)蓄积和泵出及P糖蛋白(P-gp)表达的影响。结果表明,CH(4μmol.L1)使K562/ADR细胞对ADR的敏感性增加7.43倍,逆转活性是VER的3.19倍,但对K562敏感株基本无影响。同时CH浓度依赖性地增加K562/ADR细胞内ADR和Rho123的蓄积,减少Rho123的泵出,抑制P糖蛋白的表达,但对K562细胞均无明显影响。CH在体外逆转肿瘤细胞多药耐药性的作用可能与其抑制P糖蛋白的功能和表达有关。
To study the reversal of multidrug resistance in K562 / ADR cells by cepharanthine hydrochloride (CH) and its mechanism. MTT assay was used to detect the cytotoxic effect of adriamycin (ADR) alone and in combination with CH and verapamil (VER). Flow cytometry was used to determine the effect of CH on the accumulation of ADR, Effects of Ming123 (Rho123) Accumulation and Pumping on P-glycoprotein (P-gp) Expression. The results showed that CH (4μmol.L1) increased the sensitivity of K562 / ADR cells to ADR by 7.43-fold and reversed the activity of 3.19 folds of VER, but had no effect on K562-sensitive strains. CH concentration-dependently increased the accumulation of ADR and Rho123 in K562 / ADR cells, decreased the pumping of Rho123 and inhibited the expression of P-glycoprotein, but had no significant effect on K562 cells. The role of CH in reversing the multidrug resistance of tumor cells in vitro may be related to the inhibition of the function and expression of P-glycoprotein.