A series of nanofibrous scaffolds were prepared by electrospinning of poly(vinyl alcohol) (PVA)/gelatin aqueous solution. PVA and gelatin was dissolved in pure water and blended in full range, then being electrospun to prepared nanofibers, followed by being crosslinked with glutaraldehyde vapor and heat treatment to form nanofibrous scaffold. Field emission scanning electron microscope (FESEM) images of the nanofibers manifested that the fiber average diameters decreased from 290 to 90 nm with the increasing of gelatin. In vitro degradation rates of the nanofibers were also correlated with the composition and physical properties of electrospinning solutions. Cytocompatibility of the scaffolds was evaluated by cells morphology and MTT assay. The FESEM images revealed that NIH 3T3 fibroblasts spread and elongated actively on the scaffolds with spindle-like and star-type shape. The results of cell attachment and proliferation on the nanofibrous scaffolds suggested that the cytotoxicity of all samples are grade 1 or grade 0, indicating that the material had sound biosafety as biomaterials. Compared with pure PVA and gelatin scaffolds, the hybrid ones possess improved biocompatibility and controllability. These results indicate that the PVA/gelatin nanofibrous have potential as skin scaffolds or wound dressing.
Background: Compared with titanium (Ti) and other metal implant materials, poly(ether-ether ketone) (PEEK) shows outstanding biomechanical properties. A number of studies have also reported attractive bioactivity for nano-TiO 2 (n-TiO 2 ). Methods: In this study, n-TiO 2 /PEEK nanocomposites were prepared, taking advantage of the unique properties of both PEEK polymer and n-TiO 2 . The in vitro and in vivo bioactivity of these nanocomposites was assessed against a PEEK polymer control. The effect of surface morphology or roughness on the bioactivity of the n-TiO 2 /PEEK nanocomposites was also studied. n-TiO 2 /PEEK was successfully fabricated and cut into disks for physical and chemical characterization and in vitro studies, and prepared as cylindrical implants for in vivo studies. Their presence on the surface and dispersion in the composites was observed and analyzed by scanning and transmission electron microscopy and X-ray photoelectron spectroscopy. Results: Bioactivity evaluation of the nanocomposites revealed that pseudopods of osteoblasts preferred to anchor at areas where n-TiO 2 was present on the surface. In a cell attachment test, smooth PEEK showed the lowest optical density value (0.56 ± 0.07) while rough n-TiO 2 /PEEK exhibited the highest optical density value (1.21 ± 0.34, P , 0.05). In in vivo studies, the percent bone volume value of n-TiO 2 /PEEK was approximately twice as large as that of PEEK (P , 0.05). Vivid three-dimensional and histologic images of the newly generated bone on the implants further supported our test results. Conclusion: Our study demonstrates that n-TiO 2 significantly improves the bioactivity of PEEK, especially if it has a rough composite surface. A n-TiO 2 /PEEK composite with a rough surface could be a novel alternative implant material for orthopedic and dental applications.
CYLD negatively regulates the NF-κB signaling pathway and osteoclast differentiation largely through antagonizing TNF receptor-associated factor (TRAF)-mediated K63-linkage polyubiquitination in osteoclast precursor cells. CYLD activity is controlled by IκB kinase (IKK), but the molecular mechanism(s) governing CYLD protein stability remains largely undefined. Here, we report that SCFβ-TRCP regulates the ubiquitination and degradation of CYLD, a process dependent on prior phosphorylation of CYLD at Ser432/Ser436 by IKK. Furthermore, depletion of β-TRCP induced CYLD accumulation and TRAF6 deubiquitination in osteoclast precursor cells, leading to suppression of RANKL-induced osteoclast differentiation. Therefore, these data pinpoint the IKK/β-TRCP/CYLD signaling pathway as an important modulator of osteoclastogenesis.
These findings demonstrate the anti-inflammatory activity of BTZ against periodontal inflammatory response and present BTZ as a promising therapy for periodontal disease.
Autophagy and nf-κB signaling are involving in the process of Particle Disease, which was caused by the particles released from friction interface of artificial joint, implant materials of particle reinforced composite, scaffolds for tissue engineering, or material for drug delivery. However, the biological interaction of different material particles and the mechanism of proteasome inhibitor, Bortezomib (BTZ), against Titanium (Ti) particle-induced Particle Disease remain unclear. In this study, we evaluated effect of nanosized Alumina (Al) particles and BTZ on reducing and treating the Ti particle-induced inflammatory reaction in MG-63 cells and mouse calvarial osteolysis model. We found that Al particles and BTZ could block apoptosis and NF-κB activation in osteoblasts in vitro and in a mouse model of calvarial resorption induced by Ti particles. We found that Al particles and BTZ attenuated the expression of inflammatory cytokines (IL-1β, IL-6, TNF-α). And Al prevented the IL-1β expression induced by ti via attenuating the nf-κB activation β-TRCP and reducing the expression of Casepase-3. Expressions of autophagy marker LC3 was activated in Ti group, and reduced by Al and/ not BTZ. Furthermore, the expressions of OPG were also higher in these groups than the Ti treated group. Collectively, nanosized Al could prevent autophagy and reduce the apoptosis, inflammatory and osteolysis induced by Ti particles. Our data offered a basic data for implant design when it was inevitable to use Ti as biomaterials, considering the outstanding mechanical propertie of Ti. What's more, proteasome inhibitor BTZ could be a potential therapy for wear particle-induced inflammation and osteogenic activity via regulating the activity of NF-κB signaling pathway.
Ti-μ implant particle residual was more toxic than Al-n implant particle residual. Al-n and BTZ prevented the Particle Disease induced by Ti-μ via blocking inflammation in vitro and aseptic bone loosening in vivo.
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