No abstract

Graphene oxide (GO) has attracted great interest in many different areas, as a delivery vehicle for antibacterial agents and has shown high potential. Although silver nanoparticles (AgNPs) have strong antibacterial effect, the biological application of AgNPs is often hindered by their aggregation and low stability. In this study, we developed an approach of polyoxyethylene bis (amine) (PEG) directed AgNPs grown on GO, then we combined the two materials to prepare a series of functionalized GO bearing different size AgNPs, and studied the size effects of AgNPs on growth inhibition of Escherichia coli (E.coli) and Staphylococcus aureus (S.aureus). We evaluated the antibacterial effect of GO@PEG@AgNPs on E.coli and 16 loaded on a greater number of GO, the higher will be the load efficiency, so that smaller-sized AgNPs show stronger antibacterial activity.The time-and concentration-dependent antibacterial effects of the four GO@PEG@AgNPs composites were evaluated by OD 600 . As shown in Fig 4B, before treatment with the four composites, the OD 600 value of E. coli was 0.77 and that of S. aureus 0.85. Furthermore, after treatment with 10 µg/mL GO@PEG@AgNPs composites for 4 h, the OD 600 of E. coli decreased to 0.2 (Fig 4Ba), indicating almost no E. coli survival, whereas the OD 600 of S. aureus was 0.4 (Fig 4Bb), indicating that the cytotoxicity of GO@PEG@Ag composites were greater to E. coli than to S. aureus. We also observed the same trend in concentration dependence (Fig 3S) of toxicity to E. coli and S. aureus treated with the four composites. As shown in Fig 4A, for each composite, the number of surviving E. coli was smaller than that of surviving S. aureus. Moreover, in the group treated with 10 nm GO@PEG@AgNPs, nearly no E. coli bacterial colony on the LB agar plate was formed, and only a few E. coli cells remained viable in the treated culture, markedly lower than the number of viable S. aureus cells. This result may be because of the greater thickness of gram-positive than gram-negative bacteria cell walls. Ca 2+ and Mg 2+ can decrease the antibacterial activity of GO@PEG@AgNPsTo investigate the effect of 10 nm GO@PEG@AgNPs on the bacterial surface, various metallic ions such as Zn 2+ , Cu 2+ , K + , Na + , Ca 2+ , and Mg 2+ on bacterial suspensions were investigated. The results revealed that the OD600 of E.coli clearly increased when Ca 2+ and Mg 2+ were added to the bacterial suspensions, indicating that the antimicrobial activity of the nanoparticles decreased (Fig 5). Antibacterial Fig 4. Viable bacteria remaining in the LB-agar plates of E. coli and S.aureus after being treated with four types GO@PEG@AgNPs respectively (A) (a and f are control groups, b and g are 80 nm, c and h are 50 nm, d and i are 30 nm, e and j are 10 nm), Effect of time antibacterial activity (B) of four types GO@PEG@AgNPs represented by OD600 for (a) E. coli and (b) S. aureus.

Stem cells have generated a great deal of excitement in tissue engineering and regenerative medicine, and it is important to understand the interaction mechanisms between nanomaterials and mesenchymal stem cells (MSCs) for biomedical applications. In this study, ruthenium (II) functional selenium nanoparticles (Ru@Se) are used for stem cell research. Specifically, Ru@Se are compared with citric acid selenium nanoparticles (Cit@Se)to identify their effects on MSCs differentiation and associated molecular mechanism. These data suggest that the effective adsorbing abilities of Ru@Se and Cit@Se allow them to act as preconcentration materials for osteogenic chemical inducers, which accelerates MSCs differentiation into osteoblasts. Further results suggest that selenium nanoparticles enhance the differentiation of MSCs toward osteogenic lineage over adipocytes by promoting osteogenic transcription and attenuating adipogenic transcription. Ru@Se and Cit@Se exert these effects by activating Smad‐dependent BMP signaling pathway, which regulates the expression of relevant genes to induce osteogenic differentiation.

Although clay-based nanocomposite hydrogels have been widely explored, the instability of them in hot water and saline solution inhibit their applications in biomedical engineering, and the exploration of clay-based nanocomposite...

Stem cells are well-known for their great capacity for tissue regeneration. This provides a promising source for cell-based therapies in treating various bone degenerative disorders. However, the major hurdles for their application in transplantation are the poor bone marrow homing and engraftment efficiencies. Stromal cell-derived factor 1 (SDF-1) has been identified as a major stem cell homing factor. With the aims of bone targeted SDF-1 delivery and regulating MSCs migration, alendronate modified liposomal nanoparticles (Aln-Lipo) carrying SDF-1 gene were developed in this study. Alendronate modification significantly increased the mineral binding affinity of liposomes, and facilitated the gene delivery to osteoblastic cells. Up-regulated SDF-1 expression in osteoblasts triggered MSCs migration. Systemic infusion of Aln-Lipo-SDF-1 with fluorescence labeling in mice showed the accumulation in osseous tissue by biophotonic imaging. Corresponding to the delivered SDF-1, the transplanted GFP MSCs were attracted to bone marrow and contributed to bone regeneration. This study may provide a useful technique in regulating stem cell migration.

A neuropathological hallmark of Alzheimer's disease (AD) is aggregation of a forty-residue peptide known as amyloid beta forty (Aβ40). While past work has indicated that blocking Aβ40 aggregation could be an effective strategy for the treatment of AD, developing therapies with this goal has been met with limited success. Polyoxometalates (POMs) have been previously investigated for their anti-viral and anti-tumoral properties and we report here that three representative POM nanoclusters have been synthesized for use against Aβ40 aggregation. Through the use of thioflavin T fluorescence, turbidity, circular dichroism spectroscopy, and transmission electron microscopy (TEM), we found that all three POM complexes can significantly inhibit both natural Aβ40 self-aggregation and metal-ion induced Aβ40 aggregation. We also evaluated the protective effect of POM complexes on Aβ40-induced neurotoxicity in cultured PC12 cells and found that treatment with POM complexes can elevate cell viability, decrease levels of intracellular reactive oxygen species, and stabilize mitochondrial membrane potential. These findings indicate that all three representative POM complexes are capable of inhibiting Aβ40 aggregation and subsequent neurotoxicity. While a complete mechanistic understanding remains to be elucidated, the synthesized POM complexes may work through a synergistic interaction with metal ions and Aβ40. These data indicate that POM complexes have high therapeutic potential for use against one of the primary neuropathological features of AD.

No abstract

The interaction of ruthenium (II) complex [Ru(bpy)2(mal)](2+) (RBM) and [Ru(phen)2(mal)](2+) (RPM) (bpy = 2, 2-bipyridine, phen = 1,10-phenanthroline, mal = malonyl carboxylate) with human serum albumin (HSA) has been investigated by using fluorescence, UV absorption and circular dichroism (CD) spectroscopy approaches. A strong fluorescence quenching reaction of complexes to HSA was observed and the quenching mechanism was suggested as static quenching according to the Stern-Volmer (S-V) equation. The number of binding sites n and observed binding constant Kb was measured by fluorescence quenching method. The thermodynamic parameters ΔH, ΔS, and ΔG at different temperatures were calculated and the results indicate the binding reaction is mainly entropy-driven and Vander Waals force played a major role in the reaction. The result of CD showed that the secondary structure of HSA molecules was changed in the presence of the ruthenium (II) complexes. Furthermore, the cell viability of ruthenium (II) complexes was evaluated by MTT and complex RPM has shown significant higher anticancer potency than RBM against all the cell lines screened. RPM showed a significant antitumor activity through induction of apoptosis in A549 cells.