A polymer of Galactosamine-hyaluronic acid-Vitamin E succinate (Gal-HA-VES) was designed to prepare multifunctional self-assembled micelles for delivery of Norcantharidin (NCTD) to Hepatic carcinoma. NCTD/Gal-HA-VES showed higher cytotoxicity toward CD44-overexpressing MCF-7 cells, MCF-7/Adr cells and ASGP-R overexpressing HepG2 cells, consistent with the enhanced cellular uptake in the selected cell models, indicating Gal-HA-VES micelles were taken up in MCF-7 and HepG2 cells by CD44 and ASGPR receptor mediated endocytosis, respectively. Moreover, the accumulation of Rhodamine 123 demonstrated that Gal-HA-VES has the same action of TPGS as a P-glycoprotein inhibitor blocked drug efflux-related MDR mechanism in resistant MCF-7/Adr cells. The Cell apoptosis assays indicated that NCTD/Gal-HA-VES were more effective in triggering apoptosis, compared with free NCTD or NCTD/HA-VES groups. In vivo study demonstrated that NCTD/Gal-HA-VES group exhibited enhanced tumor targeting and antitumor activity with lower systemic toxicity. Hence NCTD/Gal-HA-VES micelles system can achieve significant tumor targeting and effective treatment of hepatic carcinoma.

设计半乳糖胺-透明质酸-维生素E琥珀酸酯（Gal-HA-VES）的聚合物，以制备多功能的自组装胶束，以将降冰素（NCTD）递送至肝癌。NCTD / Gal-HA-VES对CD44过表达的MCF-7细胞，MCF-7 / Adr细胞和ASGP-R过表达的HepG2细胞显示出更高的细胞毒性，这与所选细胞模型中细胞摄取的增加相一致，表明Gal-HA- VES胶束分别通过CD44和ASGPR受体介导的内吞作用吸收在MCF-7和HepG2细胞中。此外，若丹明123的积累表明Gal-HA-VES与TP具有与TPGS相同的作用-糖蛋白抑制剂在耐药的MCF-7 / Adr细胞中阻断了与药物外流相关的MDR机制。细胞凋亡试验表明，与游离NCTD或NCTD / HA-VES组相比，NCTD / Gal-HA-VES更有效地触发了细胞凋亡。体内研究表明，NCTD / Gal-HA-VES组表现出增强的肿瘤靶向性和抗肿瘤活性，并具有较低的全身毒性。因此，NCTD / Gal-HA-VES胶束系统可以实现显着的肿瘤靶向和肝癌的有效治疗。