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本文以抗阿霉素（ADM）的人肺腺癌A549细胞亚侏A549／R1和A549／R2为模型，对异搏定（VPL）的体外逆转化疗抗药性效果及作用机理进行了初步探讨。发现VPL浓度在10μ/ml以下时无直接抑癌作用；以10μg/ml剂量VPL与ADM联合，能使A549／R2细胞内ADM聚积量显著增加，并能使抗药细胞的抗药指数显著下降；VPL的这些作用与其钙通道阻滞功能无关。结果表明，VPL在体外能有效地逆转肺腺癌细胞的抗药性，此作用与VPL同P-糖蛋白竞争性结合，阻止药物外排有关，与钙通道无关。
In this study, the antitumor effect of verapamil (VPL) in vitro and its mechanism of action were investigated by using A549 cell adenovirus A549/R1 and A549/R2 as adriamycin (ADM). It was found that the concentration of VPL below 10μ/ml had no direct tumor suppressor effect; the combination of VPL at a dose of 10μg/ml with ADM could significantly increase the accumulation of ADM in A549/R2 cells, and could significantly reduce the drug resistance index of drug-resistant cells. These effects of VPL have nothing to do with its calcium channel blocking function. The results showed that VPL can effectively reverse the drug resistance of lung adenocarcinoma cells in vitro. This effect is in combination with VPL and P-glycoprotein, which prevents drug efflux and has nothing to do with calcium channels.