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基于金纳米粒子或金纳米棒功能化的 DNA 修饰水凝胶微胶囊的热致等离子体触发负载释放。

Thermoplasmonic-Triggered Release of Loads from DNA-Modified Hydrogel Microcapsules Functionalized with Au Nanoparticles or Au Nanorods.

机构信息

Institute of Chemistry, The Minerva Center for Complex Bio-Hybrid System, The Hebrew University of Jerusalem, Jerusalem, 91904, Israel.

Institute of Life Science, The Hebrew University of Jerusalem, Jerusalem, 91904, Israel.

出版信息

Small. 2020 Jun;16(22):e2000880. doi: 10.1002/smll.202000880. Epub 2020 May 6.

DOI:10.1002/smll.202000880
PMID:32374508
Abstract

Microcapsules consisting of hydrogel shells cross-linked by glucosamine-boronate ester complexes and duplex nucleic acids, loaded with dyes or drugs and functionalized with Au nanoparticles (Au NPs) or Au nanorods (Au NRs), are developed. Irradiation of Au NPs or Au NRs results in the thermoplasmonic heating of the microcapsules, and the dissociation of the nucleic acid cross-linkers. The separation of duplex nucleic acid cross-linkers leads to low-stiffness hydrogel shells, allowing the release of loads. Switching off the light-induced plasmonic heating results in the regeneration of stiff hydrogel shells protecting the microcapsules, leading to the blockage of release processes. The thermoplasmonic release of tetramethylrhodamine-dextran, Texas Red-dextran, doxorubicin-dextran (DOX-D), or camptothecin-carboxymethylcellulose (CPT-CMC) from the microcapsules is introduced. By loading the microcapsules with two different drugs (DOX-D and CPT-CMC), the light-controlled dose release is demonstrated. Cellular experiments show efficient permeation of Au NPs/DOX-D or Au NRs/DOX-D microcapsules into MDA-MB-231 cancer cells and inefficient uptake by MCF-10A epithelial breast cells. Cytotoxicity experiments reveal selective thermoplasmon-induced cytotoxicity of the microcapsules toward MDA-MB-231 cancer cells as compared to MCF-10A cells. Also, selective cytotoxicity towards MDA-MB-231 cancer cells upon irradiation of the Au NPs- and Au NRs-functionalized microcapsules at λ = 532 or 910 nm is demonstrated.

摘要

开发了由通过葡糖胺硼酸酯复合物交联的水凝胶壳和双链核酸组成的微胶囊,负载有染料或药物,并功能化有金纳米粒子(Au NPs)或金纳米棒(Au NRs)。Au NPs 或 Au NRs 的辐照导致微胶囊的热等离子体加热和核酸交联剂的解离。双链核酸交联剂的分离导致低刚性水凝胶壳,允许负载物释放。关闭光诱导的等离子体加热导致刚性水凝胶壳的再生,保护微胶囊,导致释放过程受阻。从微胶囊中引入四甲基罗丹明-葡聚糖、Texas Red-葡聚糖、阿霉素-葡聚糖(DOX-D)或喜树碱-羧甲基纤维素(CPT-CMC)的热等离子体释放。通过将微胶囊装载两种不同的药物(DOX-D 和 CPT-CMC),实现了光控剂量释放。细胞实验表明,Au NPs/DOX-D 或 Au NRs/DOX-D 微胶囊能够有效地进入 MDA-MB-231 癌细胞,而 MCF-10A 上皮乳腺癌细胞则难以摄取。细胞毒性实验表明,与 MCF-10A 细胞相比,微胶囊对 MDA-MB-231 癌细胞具有选择性的热等离子体诱导细胞毒性。此外,还证明了在 λ = 532 或 910nm 下辐照 Au NPs 和 Au NRs 功能化的微胶囊对 MDA-MB-231 癌细胞具有选择性的细胞毒性。

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