中文摘要：

目的：制备131 I标记的、抗西妥昔单克隆抗体（ C225）修饰的免疫纳米脂质体131 I-C225-BSA-PCL，探讨其体外抑制EGFR过表达肿瘤细胞生长的作用。方法分别构建EGFR靶向性和非靶向性纳米脂质体C225-BSA-PCL和BSA-PCL，并行透射电镜和动态光散射分析；使用流式细胞仪和激光扫描共聚焦显微镜观察上述纳米脂质体在EGFR过表达肿瘤细胞中的靶向性结合及内吞情况。用氯胺T直接标记法对纳米脂质体进行131 I标记，MTT法检测131 I标记纳米脂质体的细胞杀伤活性，并观察其细胞摄取及胞内存留情况。采用独立样本t检验对数据进行分析。结果成功构建EGFR靶向性和非靶向性纳米脂质体C225-BSA-PCL和BSA-PCL，其有效直径约为130～180 nm。流式细胞仪检测和共聚焦显微镜观察结果均显示C225-BSA-PCL能被EGFR过表达的肿瘤细胞摄取，而BSA-PCL的摄取相对较弱。 MTT检测结果显示，靶向性核素纳米脂质体131 I-C225-BSA-PCL较非靶向性的131 I-BSA-PCL具有更强的细胞杀伤效果，IC50值分别为0．03～1．32和0．25～12．19。细胞摄碘实验结果显示，131 I-C225-BSA-PCL能被细胞快速摄取，并于4 h达摄取峰值，其细胞摄取明显高于131 I-BSA-PCL（ t＝3．03～16．86，均P＜0．05）。结论 EGFR靶向性纳米脂质体C225-BSA-PCL较BSA-PCL具有更强的与EGFR过表达肿瘤细胞结合并被其摄取的能力。131 I-C225-BSA-PCL可在EGFR过表达的肿瘤细胞中存留较长时间并表现出明显的靶向性杀伤效果，能有效抑制肿瘤细胞的生长。

英文摘要：

Objective To construct 131 I labeled anti-EGFR immunoliposome nanoparticle （ 131 I-Cetuaximab （ C225）-BSA-PCL） , and investigate its inhibitory effect on EGFR-overexpressing cancer cells in vitro. Methods Anti-EGFR liposome nanoparticle C225-BSA-PCL and non-targeted liposomes BSA-PCL were constructed. The products were observed with transmission electron microscopy and dynamic light scat？tering. The EGFR-targeted binding and cellular uptake in EGFR-overexpressing cancer cells were observed with flow cytometry and confocal microscopy. Anti-EGFR and non-targeted liposomes were labeled with 131 I using the chloramine-T method. The targeted cell killing effects of 131 I labeled liposomes were analyzed using MTT assay. The time-dependent cellular uptake analysis was used to evaluate the slow-release effects of the 131 I labeled liposomes. The independent？samples t test was used for data analysis. Results The EG-FR-targeted liposome C225-BSA-PCL and non-targeted liposome BSA-PCL were successfully constructed, and the effective diameters were approximately 130-180 nm. Flow cytometry and confocal microscopy re-vealed significant uptake of C225-BSA-PCL in EGFR-overexpressing tumor cells. BSA-PCL could also bind to cells with minimal and weak tumor retention. The EGFR-targeted radioactive liposome 131I-C225-BSA-PCL showed greater targeted cell killing effect than non-targeted liposome 131I-BSA-PCL,the IC50 values of 131I-C225-BSA-PCL and 131 I-BSA-PCL were 0. 03-1. 32 and 0. 25-12. 19, respectively. The uptakes of 131 I-C225-BSA-PCL was higher than that of 131 I-BSA-PCL （ t=3.03-16.86, all P〈0.05） and reached the maxi-mal level at 4 h after incubation. Conclusions The EGFR-targeted liposome C225-BSA-PCL demonstrated superior cellular binding and uptake on EGFR-overexpressing cancer cells compared with BSA-PCL. The EGFR-targeted radioactive liposome 131 I-C225-BSA-PCL had favorable intracellular retention and excellent targeted cell killing effect, and could effectively suppress the growth of EGFR-overexpr