| 杨辰,朱然,万建美,周大勇,宋妙丽,高菲,刘芬菊.125I-UdR壳聚糖纳米微粒对肝癌细胞的内照射生物学效应[J].中华放射医学与防护杂志,2015,35(5):323-328 |
| 125I-UdR壳聚糖纳米微粒对肝癌细胞的内照射生物学效应 |
| Biological effects of 125I-UdR chitosan nanoparticles on hepatoma cells |
| 投稿时间：2014-03-27 |
| DOI：10.3760/cma.j.issn.0254-5098.2015.05.002 |
| 中文关键词: 125I-UdR-壳聚糖-载药纳米微粒 肝癌 被动靶向 |
| 英文关键词:125I-UdR-chitosan-nanoparticles Liver cancer Passive targeting |
| 基金项目:国家自然科学基金(30870585,31270897,81302383);江苏省重点高校学术发展计划(PAPD) |
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| 中文摘要: |
| 目的 评估125I-UdR壳聚糖载药纳米微粒(125I-UdR-CS-DLN)对肝癌细胞的内照射生物学效应.方法 采用激光共聚焦显微镜观察125I-UdR-CS-DLN在肝癌细胞HepG2和人正常肝组织细胞HL-7702内的聚积和分布;通过MTT实验、流式细胞仪和单细胞凝胶电泳技术,评价内照射细胞生物学效应;采用TUNEL染色法观察兔肝原位肿瘤细胞经125I-UdR-CS-DLN靶向治疗后的细胞凋亡.结果 纳米微粒作用30 min后,其在HepG2细胞质内的聚积大于HL-7702;当125I-UdR-CS-DLN浓度大于37 kBq/ml时,HepG2细胞在纳米微粒作用后24、48 h的存活率显著低于HL-7702细胞(t=-4.46~6.31,P<0.05),且细胞周期G1期阻滞明显, G2/M期细胞明显受损;125I-UdR-CS-DLN造成细胞DNA双链断裂的程度明显高于125I-UdR,HepG2细胞的DNA损伤后修复能力显著低于HL-7702(Olive尾矩:t=2.94,P<0.05;彗尾DNA%:t=10.64,P<0.01);兔肝原位癌模型经介入被动靶向治疗后的TUNEL染色结果表明,125I-UdR-CS-DLN可使兔肝原位肿瘤细胞产生明显的凋亡,而相同剂量125I-UdR作用后肿瘤并未出现明显的凋亡.结论 125I-UdR-CS-DLN进入肝癌细胞的能力明显强于125I-UdR,引起的DNA辐射损伤效应更强,可明显加剧肝癌细胞的凋亡,阻止DNA损伤修复. |
| 英文摘要: |
| Objective To evaluate the internal irradiation biological effects of 125I-UdR chitosan nanoparticles in hepatoma cells. Methods The accumulation and distribution of 125I-UdR-CS-DLN in hepatoma cells HepG2 and human liver tissue cells HL-7702 were observed with a confocal microscopy. The internal irradiation biological effects were evaluated by MTT assay, flow cytometry and single cell gel electrophoresis. The apoptosis of in situ rabbit liver tumor treated with 125I-UdR-CS-DLN was assayed by TUNEL staining technique. Results After 30 min of nano-particle treatment, its accumulation in the cytoplasm of HepG2 cells was significantly greater than that in HL-7702 cells. When the concentrations of 125I-UdR-CS-DLN was higher than 37 kBq/ml, the cell viability of HepG2 was significantly lower than that of HL-7702 at 24 and 48 h post-treatment(t=-4.46-6.31,P<0.05), and the HepG2 cells were arrested at G1 phase and significantly impaired at G2/M phase. In addition, the degrees of DNA double-strand break of both cell lines irradiated by 125I-UdR-CS-DLN were significantly higher than those treated with 125I-UdR, and the DNA repair capacity of HepG2 cells was significantly lower than that of HL-7702 cells(OTM:t=2.94,P<0.05;TDNA%:t=10.64,P<0.01). TUNEL staining showed that cell apoptosis could be induced in the rabbit liver carcinoma by 125I-UdR-CS-DLN but not by 125I-UdR.Conclusions The amount of 125I-UdR-CS-DLN absorbed by hepatoma cells is significantly higher than that of 125I-UdR, which suggests that 125I-UdR-CS-DLN induces more stronger internal radiation biological effects of apoptosis and DNA damage on hepatoma cells. |
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