脂质体包裹的阿糖胞苷三磷酸（AraCTP）在体外克服小鼠淋巴瘤中的阿糖胞苷（AraC）耐药性。
Liposomally trapped AraCTP to overcome AraC resistance in a murine lymphoma in vitro.
作者信息
Richardson V J, Curt G A, Ryman B E
出版信息
Br J Cancer. 1982 Apr;45(4):559-64. doi: 10.1038/bjc.1982.92.
Two cell lines, one sensitive and one resistant to the cytotoxic effects of cytosine arabinoside (AraC) were studied in vitro as a drug-resistance model. The sensitivity of these cell lines, to the effects of free and liposomally trapped AraC and AraCTP as well as empty liposomes alone and mixed with free drug, was studied. This was done by following the inhibition of [3H]-dT incorporation into cellular DNA during exposure to the various drugs and liposomes. Some of the liposomal-lipid compositions inhibited [3H]-dT incorporation at very low concentrations, which made them unsuitable for further study. Liposomes composed of a 7:2:1 molar ratio of phosphatidylcholine:cholesterol:phosphatidic acid were selected as a suitable non-inhibitory carrier. Sensitivity of the two cell lines to free AraC differed by 3 logs, when compared in the [3H]-dT-incorporation assay. The resistant cell line was studied further, and was found to be up to 2 logs more sensitive to AraCTP when given in liposomes than to either the free drug alone or mixed with empty liposomes. It appears from these studies that liposomes are able to help overcome drug resistance in this cell line in vitro.
作为一种耐药模型，在体外研究了两种细胞系，一种对阿糖胞苷（阿糖胞苷）的细胞毒性作用敏感，另一种具有耐药性。研究了这些细胞系对游离型和脂质体包裹型阿糖胞苷及阿糖胞苷三磷酸的作用的敏感性，以及单独的空脂质体以及与游离药物混合的空脂质体的作用。这是通过在暴露于各种药物和脂质体期间跟踪[3H]-胸苷掺入细胞DNA的抑制情况来完成的。一些脂质体脂质组合物在非常低的浓度下就抑制了[3H]-胸苷掺入，这使得它们不适合进一步研究。由磷脂酰胆碱：胆固醇：磷脂酸摩尔比为7:2:1组成的脂质体被选为合适的非抑制性载体。在[3H]-胸苷掺入试验中比较时，两种细胞系对游离阿糖胞苷的敏感性相差3个对数。对耐药细胞系进行了进一步研究，发现当脂质体给药时，其对阿糖胞苷三磷酸的敏感性比单独使用游离药物或与空脂质体混合时高2个对数。从这些研究看来，脂质体在体外能够帮助克服该细胞系中的耐药性。
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