详细信息

A reduction-triggered nanocarrier based on host-guest interaction between pillar[5]arene derivative and viologen on MSN for intracellular delivery  ( SCI-EXPANDED收录)  

文献类型:期刊文献

英文题名:A reduction-triggered nanocarrier based on host-guest interaction between pillar[5]arene derivative and viologen on MSN for intracellular delivery

作者:Xu, Jun;Liu, Yehong;Li, Gaoyang;Peng, Mingxia;Xu, Shouhong[1];Liu, Honglai

机构:[1]East China Univ Sci & Technol, Shanghai Engn Res Ctr Hierarch Nanomat, Key Lab Adv Mat, Shanghai 200237, Peoples R China; East China Univ Sci & Technol, Sch Chem & Mol Engn, Shanghai 200237, Peoples R China

年份:2022

卷号:68

外文期刊名:JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY

收录:;WOS:【SCI-EXPANDED(收录号:WOS:000788084100007)】;

基金:Acknowledgement This work was supported by the National Natural Science Foundation of China (No. 22078087 and No. 21776071) . The authors also wish to thank Miss Gangmei Tang for her advice on drawing graphs and Wanshi Tang for help with language.

语种:英文

外文关键词:Intracellular delivery; Mesoporous silica nanoparticles; Host-guest interaction; Controlled drug release

摘要:Due to the difference of intracellular microenvironment between tumour and normal cells, stimuli-responsive supramolecular assemblies have been widely designed for accurate drug delivery and controlled release. This study introduces a reduction-triggered drug delivery system that encapsulates drugs in mesoporous silica nanomaterials (MSNs) pores using a supramolecular nanovalve based on host-guest interactions between pillar [5]arene and viologen groups. PEGylated pillar[5]arene (the host) can encircle viologen stalks (the guest), which have been grafted onto the MSNs surface in advance, and separate from viologen when it encounters a reducing agent. In vitro drug release experiments were conducted under various pH conditions and reducing environments to control drug release. Furthermore, cytotoxicity studies revealed that the drug-loaded nanoparticles exhibited low cytotoxicity to LO2 cells but effectively induced apoptosis in HepG2 cells. This work contributes to the development of targeted intracellular drug delivery in tumour clinical therapy.

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