敏药碱-G逆转肿瘤细胞多药耐药的作用和机制研究

目的　将敏药碱- G作用于K5 6 2 /ADM细胞,来逆转肿瘤细胞的多药耐药,研究其逆转作用和机制。方法　四唑盐比色法(MTT法)检测阿霉素对K5 6 2 /ADM细胞的半数抑制浓度(IC5 0 ) ;逆转录聚合酶链式反应(RT- PCR)检测mdr1基因水平;流式细胞仪分析细胞内罗丹明(Rh12 3)浓度,以检测P 170泵功能;免疫组化方法检测P 170的表达水平。结果　MTT结果显示,无毒剂量的敏药碱 G与ADM联合应用比单纯加ADM(同等剂量)对K5 6 2 /ADM细胞的IC5 0降低了5. 0 1倍;耐药靶细胞内罗丹明(Rh12 3)积累增加;但加敏药碱 -G前后mdr1基因与P gp表达没有明显变化。结论　敏药碱- G逆转耐药的机制可能是它抑制了P -gp的“药物泵”功能,使细胞内药物积累增加,而对mdr1基因和P- gp表达则无明显影响。

Study of effect and mechanism of MYJ-G reversing tumour cells MDR

Objective To investigate effect and functional mechanism of Chinese drug MYJ-G reversing multidrug resistance of tumor cell. Methods MTT assay determine IC50 of ADM acting on K562/ADM; RT-PCR assay detect mdr1 gene level; FCM analyse intracellular Rh123 concentration to assess p-170 function; Immunity histochemistry determine expressional level of p-170. Results MTT assay showed that IC50 of K562/ADM in MYJ-G used group was reduced 5.01 times compared with that in MYJ-G non-used group; FCM indicated that intracellular Rh123 concentration was improved after MYJ-G was used on K562/ADM; However, RT-PCR and immunity histochemistry indicated that mdr1 gene and P-gp expression were not distinctly changed after MYJ-G was used. Conclusion Mechanism of Chinese drug MYJ-G reversing multidrug resistance could be that it inhibits "drug pump" function of P-gp so as to make intracellular drug accumulation increased, but it does not affect mdr1 gene and P-gp expression level.