载阿霉素红细胞膜壳聚糖靶向纳米粒的制备及评价 点击下载
论文标题: 载阿霉素红细胞膜壳聚糖靶向纳米粒的制备及评价
英文标题:
中文摘要: 目的 制备靶向肿瘤细胞叶酸(FA)受体的载阿霉素红细胞膜壳聚糖靶向纳米粒(FA-RBC-DOX-CS-NPs),并进行评价。方法采用离子交联法制备载阿霉素壳聚糖纳米粒(DOX-CS-NPs),将FA和氨基聚乙二醇磷脂(NH2-PEG2000-DSPE)通过共价连接后修饰红细胞膜,然后构建FA-RBC-DOX-CS-NPs,并对其进行表征,考察其体外释药特性、抗肿瘤活性、入胞能力(以人乳腺癌MCF-7细胞进行考察)。结果FA-RBC-DOX-CS-NPs平均粒径为(254.200±2.651)nm,多分散性指数为0.199±0.031,Zeta电位为(-10.100±0.213)mV;其在肿瘤微环境(pH6.5)中的释放速率较快。细胞实验表明,该纳米粒可抑制MCF-7细胞的增殖活力,且可提高药物的入胞效率。结论本研究成功制备了FA-RBC-DOX-CS-NPs。该纳米粒具有较好的肿瘤细胞靶向性和入胞能力,可实现药物在肿瘤细胞内富集。
英文摘要: OBJECTIVE To prepare and evalu ate doxorubicin-loaded red blood cell membrane chitosan-targeted nanoparticles of targeting tumor cell folate acid (FA)receptor(FA-RBC-DOX-CS-NPs). METHODS Doxorubicin-loaded chitosan nanoparticles (DOX-CS-NPs) were prepared by ion cross-linking method. FA and amino polyethylene glycol phospholithin (NH2- PEG2000-DSPE)were covalently linked to modify the red blood cell membrane to construct FA-RBC-DOX-CS-NPS. FA-RBC- DOX-CS-NPs were characterized and investigated on in vitro drug release characteristics ,antitumor activity and endocytosis ability (investigation with human breast cancer MCF- 7 cells). RESULTS Average particle size of FA-RBC-DOX-CS-NPs was (254.200± 2.651)nm,and polydispersity index was 0.199±0.031;Zeta potential was (-10.100±0.213)mV. FA-RBC-DOX-CS-NPs released fast in the tumor microenvironment (pH6.5). Cellular experiments showed that ,the nanoparticles could inhibit the activity of MCF- 7 cell proliferation and improve the efficiency of endocytosis. CONCLUSIONS FA-RBC-DOX-CS-NPs are prepared successfully. The nanoparticles have good tumor cell targeting and endocytosis ability ,and can realize the enrichment of drugs in tumor cells.
期刊: 2022年第33卷第13期
作者: 洪伟勇,周旭晖,金陈浩,王金明,郭钫元,杨根生
英文作者: HONG Weiyong ,ZHOU Xuhui,JIN Chenhao ,WANG Jinming ,GUO Fangyuan ,YANG Gensheng
关键字: 红细胞膜;纳米粒;叶酸受体;靶向给药系统;抗肿瘤
KEYWORDS: red blood cell membrane ;nanoparticles;folic acid receptor ;targeted drug delivery system ;anti-tumor
总下载数: 81次
本日下载数: 2次
本月下载数: 81次
文件大小: 619.60Kb

* 注:未经本站明确许可,任何网站不得非法盗链资源下载连接及抄袭本站原创内容资源!在此感谢您的支持与合作!