Supramolecular Assembly of ß-Cyclodextrin-Modified Polymer by Electrospinning with Sustained Antibacterial Activity.

Supramolecular assembly loading drug as biomedical materials is a research hotspot. Herein, we reported a supramolecular electrospun assembly constructed via the hydrophobic and hydrogen bonding interaction. The obtained results showed that the assembly by supramolecular electrospinning not only increased the interactions of multiple antibacterial active species including antibiotics, cationic polymers, and silver to form a flexible membrane with good mechanical strength but also indicated the dual effects of rapid doxycycline and polyethyleneimine release as well as a sustained Ag release. Interestingly, the assembly showed not only good degradability but also a high bacteriostatic efficacy toward Escherichia coli (E. coli) up to 99.9%. More importantly, the in vivo wound healing assay indicated that the assembly could promote the healing of uninfected, E. coli-infected, and even methicillin-resistant staphylococcus aureus-infected wounds. The current research provides a novel approach to construct a supramolecular assembly by electrospinning mechanically induced strong noncovalent interaction.

Adult Stem Cells Seeded on Electrospinning Silk Fibroin Nanofiberous Scaffold Enhance Wound Repair and Regeneration.

Development of novel strategy stimulating the healing with skin appendages regeneration is the critical goal for wound therapy. In this study, influence of the transplantation of bone marrow derived mesenchymal stem cells (MSCs) and epidermal stem cells (ESCs) with the nanofiberous scaffold prepared from silk fibroin protein in wound re-epithelization, collagen synthesis, as well as the skin appendages regeneration were investigated. It was shown that both the transplantation of MSCs and ESCs could significantly accelerate the skin re-epithelization, stimulate the collagen synthesis. Furthermore, the regenerative features of MSCs and ESCs in activating the blood vessels and hair follicles formation, respectively were suggested. These results demonstrated that the electrospinning nanofiberous scaffold is an advantageous carrier for the cells transplantation, but also provided the experimental proofs for the application of MSCs and ESCs as promising therapeutics in skin tissue engineering.

Overexpression of a laccase gene, DiLAC17, from Davidia involucrata causes severe seed abortion in Arabidopsis.

Seed abortion is a common phenomenon in woody plants, especially in rare and endangered species. Serious seed abortion occurs in the dove tree and largely restricts its natural reproduction. A number of differentially expressed genes (DEGs) between normal and aborted seeds of the dove tree have been previously identified through transcriptome profiling. Among these, most DEGs encoding laccase showed significant upregulation in the aborted seeds. In this study, the laccase gene with the highest expression level in aborted seeds, DiLAC17, was cloned from the dove tree genome and further verified. Overexpression of the DiLAC17 gene in Arabidopsis resulted in retarded growth, deformed siliques, and severe seed abortion. Most Arabidopsis genes involved in seed development, such as AtLEC2, AtANT1, and AtRGE1, were suppressed in the transgenic lines. Laccase activity and lignin content were significantly improved in transgenic lines under ectopic overexpression of the DiLAC17 gene. Excessive lignin accumulation in the early developmental stage was assumed to be a key cause of restricting silique growth and seed expansion, which ultimately led to seed abortion. These results indicate a laccase-mediated pathway for seed abortion, which might be a strategy adopted by this rare and endangered species to reduce the reproductive load.

Surface-modified PLGA nanoparticles with chitosan for oral delivery of tolbutamide.

The main purpose of present study was to develop novel chitosan-modified polylactic-co-glycolicacid nanoparticles (CS@PLGA NPs) for improving the bio-availability of tolbutamide (TOL). The TOL-loaded CS@PLGA NPs (TOL-CS@PLGA NPs) were fabricated with the solvent evaporation method. The cargo-free CS@PLGA NPs showed a diameter of 228.3±2.5nm monitored with a laser light particlesizer, and the transmission electron microscope (TEM) photographs revealed their "core-shell" structures. The Zeta potential of the original PLGA NPs and the cargo-free CS@PLGA NPs was measured to be -20.2±3.21mV and 24.2±1.1mV, respectively. The changes in Zeta potential indicated the CS chains were coated on the surfaces of the original PLGA NPs. The thermal gravity analysis (TGA) curves suggested that the CS chains improved the thermostability of the original PLGA NPs. The results of cells viability indicated the cargo-free CS@PLGA NPs were nontoxicity. The in vitro release profiles suggested that TOL-CS@PLGA NPs could release TOL in pH 7.4 phosphate buffer solution (PBS) at a sustained manner. Streptozotocin (STZ) was employed to build the diabetic rat models. The physiological changes in the islet ß cells confirmed the obtaining of diabetic rats. After treatment by gavage, the TOL-CS@PLGA NPs showed an excellent hypoglycemic effect. Therefore, the TOL-CS@PLGA NPs had a potential application in oral delivery of TOL.

Lrg participates in lipopolysaccharide preconditioning-induced brain ischemia injury via TLR4 signaling pathway.

Lipopolysaccharide (LPS) preconditioning is a powerful neuroprotective phenomenon by which an injurious stimulus renders the brain resistant to a subsequent damaging ischemic insult. The LPS response gene (Lrg) is a recently identified gene in human dental pulp cells treated with LPS. However, the role and mechanism of Lrg in brain ischemia injury have not yet been demonstrated. Here, we sought to determine whether Lrg participates in LPS preconditioning-induced brain ischemia injury. The Lrg protein accumulates in brain tissue after middle cerebral artery occlusion (MCAO). Furthermore, knockdown of Lrg by small interfering RNA (siRNA) significantly increased the infarct size of brain injury. In addition, we investigated the mechanism of Lrg in brain ischemia injury. Lrg-siRNA could regulate inflammatory cytokine expression. Moreover, interleukin-1 receptor-associated kinase 1 (IRAK-1) and nuclear factor Kappa B (NF-κB) p65 protein levels were significantly increased by Lrg-siRNA in mice after MCAO. Conversely, interferon regulatory factor 3 (IRF3) protein level was decreased by Lrg-siRNA. Taken together, these results suggest that Lrg regulates the expression of inflammatory cytokines in LPS preconditioning-induced brain ischemia injury via the toll-like receptor 4 (TLR4) signaling pathway. Lrg may therefore serve as a novel therapeutic target for brain ischemia injury.