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首页> 外文期刊>Cancer biotherapy and radiopharmaceuticals >Biological effects of irradiating hepatocellular carcinoma cells by internal exposure with 125I-labeled 5-iodo-2′-deoxyuridine-chitosan drug loading nanoparticles
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Biological effects of irradiating hepatocellular carcinoma cells by internal exposure with 125I-labeled 5-iodo-2′-deoxyuridine-chitosan drug loading nanoparticles

机译:125I标记的5-碘-2'-脱氧尿苷-壳聚糖载药纳米粒子内部暴露对肝细胞癌细胞的生物学作用

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In this study, the authors evaluate the biological effects of irradiation of hepatocellular carcinoma cells by internal exposure with 125I-labeled 5-iodo-2′-deoxyuridine (125I-UdR)-chitosan drug loading nanoparticles (125I-UdR-CS-DLN). The authors observed that accumulation of nanoparticles was significantly (p 0.05) higher in hepatocellular carcinoma cells HepG2 than normal liver cells HL-7702 after treated with 125I-UdR-CS-DLN for 30 minutes. Survival of HepG2 cells was significantly lower at 125I-UdR-CS-DLN doses higher than 37 kBq/mL (more significant in the G1 phase and G2/M phase) than the HL-7702 cells. In addition, 125I-UdR-CS-DLN induced a higher level of DNA double-strand breaks than 125I-UdR, and HepG2 cells exhibited a lower level of DNA repair when compared with HL-7702 cells. In vivo animal experiments, TUNEL staining, after targeted treatment, showed that 125I-UdR-CS-DLN induced significant cell apoptosis in rabbit hepatocellular tumors in situ than 125I-UdR infusion at the same dose. In conclusion, hepatocellular carcinoma cells were significantly irradiated with 125I-UdR-CS-DLN compared with 125I-UdR, and 125I-UdR-CS-DLN irradiation enhanced DNA damage, induced liver cancer cell apoptosis, and prevented DNA damage repair. However, evaluating the extent of damage and organ sparing in vivo should also be considered.
机译:在这项研究中,作者评估了用125I标记的5-碘-2'-脱氧尿苷(125I-UdR)-壳聚糖载药纳米颗粒(125I-UdR-CS-DLN)内部暴露对肝细胞癌细胞辐射的生物学效应。 。作者观察到,用125 I-UdR-CS-DLN处理30分钟后,肝细胞癌细胞HepG2中的纳米颗粒积累明显高于正常肝细胞HL-7702(p <0.05)。与HL-7702细胞相比,当125I-UdR-CS-DLN剂量高于37 kBq / mL时,HepG2细胞的存活率显着降低(在G1期和G2 / M期更显着)。另外,与125I-UdR相比,125I-UdR-CS-DLN诱导的DNA双链断裂水平更高,与HL-7702细胞相比,HepG2细胞的DNA修复水平更低。在体内动物实验中,靶向治疗后的TUNEL染色显示,与相同剂量的125I-UdR输注相比,125I-UdR-CS-DLN在兔肝细胞原位肿瘤中可诱导明显的细胞凋亡。总之,与125I-UdR相比,125I-UdR-CS-DLN可以显着照射肝细胞,125I-UdR-CS-DLN照射可以增强DNA损伤,诱导肝癌细胞凋亡,并阻止DNA损伤修复。但是,还应考虑评估体内的损伤程度和保留器官。

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