中文摘要：

目的：探究中频交变微电流是否可以改变人乳腺癌细胞株耐药性;针对实验结果,分析其可能机制。方法：对人乳腺癌细胞MCF-7施加不同参数中频交变微电流,选出较优参数。测定人乳腺癌细胞MCF-7及其耐药株MCF-7/Adr的IC50值。将处于对数生长期的人乳腺癌耐药细胞MCF-7/Adr接板,分为化疗药物组和联合处理组,施加不同的处理方法。CCK-8法检测以上各组细胞存活率,分析中频交变微电流对乳腺癌细胞株耐药性的影响。将处于对数生长期的人乳腺癌细胞MCF-7分为对照组和电刺激组,用激光扫描共聚焦显微镜（CLSM）定性观察荧光标记的耐药蛋白P-gp,Western blot法半定量P-gp,流式细胞仪FITC标记定量测定荧光标记的P-gp。结果：中频交变微电流能降低耐药株MCF-7/Adr的IC50和耐药指数（≥80μg/ml,协同作用）。定性、半定量和定量三种方法均显示中频交变微电流刺激后,细胞P-gp蛋白表达量均有下降趋势。结论：中频交变微电流能够增强人乳腺癌耐药细胞药物敏感性,有可能成为辅助化疗的治疗手段,其机制尚不明确,有可能是通过降低细胞P-gp的表达,抑制细胞内药物外排发挥作用的。

英文摘要：

Objective： To investigate weather micro-current at intermediate frequency（ ACIF） can change the drug resistance of human breast cancer cells,then the possible mechanism was analyzed. Methods： ACIF of different parameters was applied in human breast cancer cells of MCF-7 to choose the optimal parameters. Measuring the IC50 of MCF-7 and MCF-7/Adr. The human breast cancer cells drug resistance mutants MCF-7/Adr in logarithmic growth phase were planted in 24-well plates,then divided into chemotherapy groups and combination groups randomly,which applied different treatment. The growth inhibiting rates of MCF-7 were determined by cell counting Kit-8（ CCK-8） method to evaluate the change on drug resistance of human breast cancer cells. The human breast cancer cells MCF-7 in logarithmic growth phase were planted in 24-well plates,then we divided it into 2 groups： control groups and electrical stimulation groups. Confocal laser scanning microscope（ CLSM） was applied to observe the P-gp expression. Western blot was used to semi-quantitatively analyze the expression of P-gp. The quantitative analysis of P-gp was measured by Flow Cytometry. Results： ACIF could decrease the the IC50 and the resistance index（ RI） of MCF-7/Adr（ ≥80μg/ml,synergistic effect）. Analysis of qualitative,semi-quantitative,quantitative all showed that after applied ACIF,the expression of P-gp was downregulated（ P = 0. 44）. Conclusion： Alternating micro-current at intermediate frequency could increase the drug sensitivity,which may be applied as an effective adjuvant that enhanced chemotherapy. The possible mechanism is decrease the expression of P-gp,so as to increase of intracellular drug concentration.