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目的 研究双嘧达莫对胃癌细胞多药耐药的逆转作用。方法 逐渐递增长春新碱浓度诱导胃癌细胞株SGC790 1产生多药耐药性 (SGC790 1r)。以双嘧达莫为逆转剂 ,MTT法测定抗癌药对肿瘤细胞的杀伤作用 ;激光全聚焦显微镜测定肿瘤细胞内柔红霉素和钙离子荧光强度。结果 胃癌SGC790 1r细胞对长春新碱、柔红霉素、丝裂霉素及顺铂的耐药性分别为SGC790 1细胞的 4.46倍、14.95倍、2 1.2 0倍和 16 .0 6倍。经双嘧达莫(5 0 μg/ml)预处理 1h后 ,柔红霉素对SGC790 1r的半数抑制浓度明显下降 (P <0 .0 5 )。SGC790 1r在静息时细胞内Ca2 + 明显高于药物敏感的母细胞株SGC790 1;细胞内柔红霉素的荧光强度亦明显降低 (P <0 .0 5 )。双嘧达莫 (5 0 μg/ml)使SGC790 1r细胞内Ca2 + 明显下降 ,柔红霉素荧光强度显著提高 (P <0 .0 5 ) ;对药物敏感细胞SGC790 1无明显作用。结论 双嘧达莫增加柔红霉素在耐药细胞内的积累 ,部分逆转SGC790 1r的耐药性。
Objective To study the reversal effect of dipyridamole on multidrug resistance in gastric cancer cells. Methods Gradually increasing the concentration of vincristine induced gastric cancer cell line SGC790 1 to produce multidrug resistance (SGC790 1r). Dipyridamole was used as a reversal agent to determine the killing effect of anticancer drugs on tumor cells by MTT assay. The fluorescence intensity of daunorubicin and calcium ions in tumor cells was determined by laser-based all-focus microscopy. Results The resistance of gastric cancer SGC790 1r cells to vincristine, daunorubicin, mitomycin and cisplatin were 4.46, 14.95, 2 1.2 and 16.0 times higher than those of SGC790 1 cells, respectively. After pretreatment with dipyridamole (50 μg/ml) for 1 h, the half-inhibitory concentration of daunorubicin on SGC790 1r decreased significantly (P < 0.05). The intracellular Ca2 + of SGC790 1r at rest was significantly higher than that of the drug-sensitive parental cell line SGC790 1; the fluorescence intensity of daunorubicin in the cells was also significantly decreased (P < 0.05). Dipyridamole (50 μg/ml) significantly decreased Ca2 + in SGC790 1r cells, and the fluorescence intensity of daunorubicin was significantly increased (P < 0.05). There was no significant effect on drug-sensitive cell SGC7901. Conclusion Dipyridamole increases the accumulation of daunorubicin in drug resistant cells and partially reverses the drug resistance of SGC790 1r.