ABSTRACT
Pickering emulsions stabilized by functional nanoparticles (NPs) have received considerable attention for improving the physical stability and biological function of NPs. Herein, hydrophobic polyphenols were chosen as phenolic ligands to form metal-phenolic network (MPN) coatings on NPs (e.g., silica, polystyrene) mediated by the sono-Fenton reaction. The MPN coatings modulated the surface wettability and charges of NPs and achieved emulsification behavior for preparing Pickering emulsions with pH responsiveness and oxidation resistance. A series of polyphenols, including resveratrol, rutin, naringin, and curcumin, were used to form MPN coatings on NPs, which served as stabilizers for the engineering of functionalized oil-in-water (O/W) Pickering emulsions. This work provides a new avenue for the use of hydrophobic polyphenols to modulate NP emulsifiers, which broadens the application of polyphenols for constructing Pickering emulsions with antioxidant properties.
ABSTRACT
The design of materials that can mimic the complex yet fast actuation phenomena in nature is important but challenging. Herein, we present a new paradigm for designing responsive hydrogel sheets that can exhibit ultrafast inverse snapping deformation. Dual-gradient structures of hydrogel sheets enable the accumulation of elastic energy in hydrogels by converting prestored energy and rapid reverse snapping (<1 s) to release the energy. By controlling the magnitude and location of energy prestored within the hydrogels, the snapping of hydrogel sheets can be programmed to achieve different structures and actuation behaviors. We have developed theoretical model to elucidate the crucial role of dual gradients and predict the snapping motion of various hydrogel materials. This new design principle provides guidance for fabricating actuation materials with applications in tissue engineering, soft robotics, and active medical implants.
Subject(s)
Biomimetic Materials/chemistry , Biomimetics , Hydrogels/chemistry , Algorithms , Biomimetics/methods , Models, TheoreticalABSTRACT
Stroke is the most common cause of mortality worldwide. Post-stroke angiogenesis is of great significance to the treatment of strokes. The aim of the present study was to investigate the mechanism underlying the angiogenesis-promoting effect of microRNA126 (miR126)associated signaling pathways using a stroke model in vivo and a cell migration model in vitro. Bone marrowderived endothelial progenitor cells (EPCs) were extracted and identified using a density gradient method. Reverse transcriptionquantitative polymerase chain reaction (RTqPCR) was performed to examine the expression levels of miR126 and CXC chemokine receptor type 7 (CXCR7). Target genes of miR126 were analyzed using TargetScan software version 7.1 (www.targetscan.org/). In addition, a reporter gene assay and RTqPCR were performed to determine the target genes of miR126. The effect of miR126 on cell migration was examined using a cell migration model in vitro and a middle cerebral artery occlusion model of mice was established in vivo. The miR126 antagomirtreated EPCs were infused into stroke mice. Microvessel density, nerve function score and infarction volume were assessed. Flow cytometric analysis indicated that cluster of differentiation (CD)34, CD133 and vascular endothelial growth factor receptor 2 were partly expressed on the cell surface of bone marrowderived EPCs. In addition, the expression levels of Diacetylatedlow density lipoprotein and Ulex europaeus agglutinin 1 were positive. Stromal cellderived factor 1 (SDF-1) was identified as a target gene of miR126, which was confirmed by a reporter gene assay and RTqPCR. Cell migration examination demonstrated that the neutralizing antibody of CXCR7 blocked miR126 angomirinduced migration of EPCs. Microvessel density increased, while nerve function score and infarction volume decreased following infusion of miR-126 angomirtreated EPCs. Furthermore, miR126 angomir improved the efficacy of EPC treatment. Thus, miR126 improved the migration of EPCs via the miR126/SDF1/CXCR7 signaling pathway.
