| 季艳会,李玮,李承霞,李宁,常津,谭建.131I标记纳米脂质体靶向治疗结肠癌的实验研究[J].中华放射医学与防护杂志,2016,36(2):81-86 |
| 131I标记纳米脂质体靶向治疗结肠癌的实验研究 |
| Evaluation of the internal therapeutic effectiveness of 131I-antiEGFR-BSA-PCL in nude mice with colorectal cancer |
| 投稿时间：2015-06-26 |
| DOI：10.3760/cma.j.issn.0254-5098.2016.02.001 |
| 中文关键词: 131I 结肠癌 纳米脂质体 表皮生长因子受体 |
| 英文关键词:131I Colorectal cancer Nano-liposome Epidermal growth factor receptor |
| 基金项目:国家自然科学基金(81301244,81171372) |
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| 摘要点击次数: 2698 |
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| 中文摘要: |
| 目的 研究131I-antiEGFR-BSA-PCL对LS180细胞结肠癌裸鼠移植瘤内照射的治疗效果。方法 构建抗表皮生长因子受体(EGFR)标记的纳米脂质体及EGFR靶向性。通过荧光共聚焦显微镜、细胞摄碘实验观察纳米载体的靶向性及LS180细胞对其摄取情况。将裸鼠40只按随机数字表法分为4组,通过瘤体内注射的方式向移植瘤内分别注射74 MBq (740 MBq/ml) 131I-antiEGFR-BSA-PCL、131I-BSA-PCL、131I及相同体积的生理盐水。通过研究裸鼠体重、肿瘤体积、SPECT显像及组织病理学方法,观察纳米脂质体的抑瘤效果。结果 共聚焦实验显示,与BSA-PCL组相比,antiEGFR-BSA-PCL组细胞内绿色荧光较明显,其介导的胞吞效应显著。摄碘率实验中,LS180细胞对131I-antiEGFR-BSA-PCL的摄取率明显高于131I-BSA-PCL(t=2.77~5.40,P<0.01)。131I-antiEGFR-BSA-PCL组与131I-BSA-PCL组裸鼠肿瘤增殖均较慢,二者差异无统计学意义(P>0.05)。给药后72 h,131I-antiEGFR-BSA-PCL与131I-BSA-PCL的肿瘤摄取率分别为(21.61±1.01)和(20.58±0.65)% ID/g,均明显高于131I组(t=9.36、8.69,P<0.01)。SPECT显像显示纳米脂质体主要特异性积聚在肿瘤区。结论 131I-antiEGFR-BSA-PCL对LS180结肠癌裸鼠移植瘤有明显的抑制作用。 |
| 英文摘要: |
| Objective To investigate the biological effects of internal radiation and therapeutic effectiveness of 131I-labeled anti-epidermal growth factor receptor (EGFR) in colorectal cancer of model mice. Methods Nano-liposome characterized for EGFR-targeting was constructed. The efficacy of cellular binding and uptake of the liposome was evaluated by the analysis of confocal microscopy observation and the iodide uptake assay. After intra-tumor injections of 74 MBq (740 MBq/ml) 131I-antiEGFR-BSA-PCL, 131I-BSA-PCL, 131I or an equivalent volume of normal saline. The biological effects of internal irradiation and therapeutic efficacy of the liposomes on colorectal cancer modeled in a male BALB/c mouse were evaluated by means of tumor size, body weight, histopathology, and SPECT imaging. Results The confocal fluorescence images showed that the antiEGFR-BSA-PCL was successfully internalized into LS180 cells. The 131I uptake efficacy of 131I-antiEGFR-BSA-PCL was significantly higher than that of 131I-BSA-PCL in LS180 cells (t=2.77-5.40,P<0.01). Tumor size measurement showed that tumor growth was inhibited by the treatment with 131I-EGFR-BSA-PCL and 131I-BSA-PCL, but had no significant differences between these two groups (P>0.05). It was found that the 131I-antiEGFR-BSA-PCL was markedly taken up by the tumor and reached its uptake value of (21.61±1.01) and (20.58±0.65)%ID/g at 72 h following drug injection, which was higher than the uptake value of 131I (t=9.36, 8.69, P<0.01). SPECT imaging assay showed that, after being injected into mouse tumor, the 131I-EGFR-BSA-PCL and 131I-BSA-PCL were uniformly distributed inside the tumor. Conclusions 131I-antiEGFR-BSA-PCL obviously suppresses the development of colorectal cancer in mice. |
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