Surface modification is an effective way to improve the hemocompatibility of biomaterials. Quercetin has significant anticoagulation and antithrombotic effects, and thus it is a promising candidate agent for the surface modification of blood-contacting materials. In this study, quercetin was successfully encapsulated in tripolyphosphate–chitosan nanoparticles (TCs) based on the ionic gelation of chitosan with tripolyphosphate (TPP) anions. Then, hyaluronan acid (HA)/quercetin-loaded TPP–chitosan nanoparticle (QTCs) films, in addition to HA/TCs films, were prepared separately using an electrostatic layer-by-layer self-assembly technique. The encapsulation of quercetin in the chitosan nanoparticles was confirmed by UV spectra. The quercetin-loaded multilayer coatings were also successfully self-assembled, as confirmed by the UV spectra and contact angle measurements. Platelet adhesion experiments were carried out with platelet-enriched plasma so as to evaluate the blood compatibility of the different samples. There were many platelets on the surfaces of the glass and HA/TC-coated titanium, which were partially activated but not aggregated. Meanwhile, many more platelets were observed on the uncoated titanium surfaces, most of which developed pseudopodia. By contrast, the platelet adhesion and activation were reduced remarkably on the surface of the HA/QTC-coated titanium. These results showed that the multilayer coatings containing quercetin could act as potential biomaterials to improve the anticoagulation performance of blood-contacting materials.

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Introduction The development of nanodrug carriers utilizing tumor microenvironment has become a hotspot in reversing multidrug resistance (MDR). Materials and methods This study synthesized a redox-sensitive copolymer, Pluronic F127-disulfide bond- d -α-tocopheryl polyethylene glycol 1000 succinate (FSST), through the connection of the reduction-sensitive disulfide bond between F127 and d -α-tocopheryl polyethylene glycol 1000 succinate. This polymer could induce the elevation of reactive oxygen species (ROS) levels, ultimately resulting in cytotoxicity. Moreover, the redox-responsive mixed micelles, F127-folate (FA)/FSST/P123 (FFSSTP), based on FSST, Pluronic F127-FA, and Pluronic P123, were prepared to load paclitaxel (PTX). Results The in vitro release study demonstrated that FFSSTP/PTX accelerated the PTX release through the breakage of disulfide bond in reductive environment. In cellular experiment, FFSSTP/PTX induced significant apoptosis in PTX-resistant MCF-7/PTX cells through inhibiting adenosine triphosphate (ATP)-binding cassette proteins from pumping out PTX by interfering with the mitochondrial function and ATP synthesis. Furthermore, FFSSTP/PTX induced apoptosis through elevating the intracellular levels of ROS. Conclusion FFSSTP could become a potential carrier for the treatment of MDR tumors.

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