Low-dose chemotherapy of hepatocellular carcinoma through triggered-release from bilayer-decorated magnetoliposomes.
Low-dose chemotherapy of hepatocellular carcinoma through triggered-release from bilayer-decorated magnetoliposomes.
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DOI：
10.1016/j.colsurfb.2014.01.022
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发表时间：
2014-04-01
影响因子：
5.8
通讯作者：
Bothun, Geoffrey D.
中科院分区：
文献类型：
--
作者：
Chen, Yanjing;Chen, Yuan;Xiao, Da;Bose, Arijit;Deng, Ruitang;Bothun, Geoffrey D.
关键词：
低剂量（LD）化疗是一种很有前途的治疗策略，可以通过控制输送来改善。聚乙二醇稳定的双层修饰磁性脂质体（dML）已被设计为刺激响应性LD化疗药物递送系统，并在体外使用Huh-7肝癌细胞系进行测试。dML在脂质双层内含有疏水性超顺磁性氧化铁纳米颗粒，在水性核内含有盐酸阿霉素（DOX，2 μM）。低温透射电子显微镜和动态光散射的结构分析表明，该组件的直径约为120 nm。此外，样品由dML和裸脂质体（无纳米颗粒）的混合物组成，其分别提供双重突释和自发DOX释放曲线。细胞活力结果显示，DOX负载的dML的细胞毒性与裸dML的细胞毒性相似（约10%），这表明自发DOX泄漏具有很小的细胞毒性作用。然而，当经受生理上可接受的射频（RF）电磁场时，8小时后细胞活力降低高达40%，24小时后观察到完全细胞死亡。治疗机制是细胞内RF触发的DOX从dML释放，而不是由于通过磁损失的纳米颗粒加热引起的细胞内高热。
Low-dose (LD) chemotherapy is a promising treatment strategy that may be improved by controlled delivery. Polyethylene glycol-stabilized bilayer-decorated magnetoliposomes (dMLs) have been designed as a stimuli-responsive LD chemotherapy drug delivery system and tested in vitro using Huh-7 hepatocellular carcinoma cell line. The dMLs contained hydrophobic superparamagnetic iron oxide nanoparticles within the lipid bilayer and doxorubicin hydrochloride (DOX, 2 µM) within the aqueous core. Structural analysis by cryogenic transmission electron microscopy and dynamic light scattering showed that the assemblies were approximately 120 nm in diameter. Furthermore, the samples consisted of a mixture of dMLs and bare liposomes (no nanoparticles), which provided dual burst and spontaneous DOX release profiles, respectively. Cell viability results show that the cytotoxicity of DOX-loaded dMLs was similar to that of bare dMLs (~10%), which indicates that spontaneous DOX leakage had little cytotoxic effect. However, when subjected to a physiologically acceptable radiofrequency (RF) electromagnetic field, cell viability was reduced up to 40% after 8 h and complete cell death was observed after 24 h. The therapeutic mechanism was intracellular RF-triggered DOX release from the dMLs and not intracellular hyperthermia due to nanoparticle heating via magnetic losses.
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