Research on sintering process of tricalcium phosphate bone tissue engineering scaffold based on three-dimensional printing / 生物医学工程学杂志

Tricalcium phosphate (TCP) is one of the most widely used bioceramics for constructing bone tissue engineering scaffold. The three-dimensional (3D) printed TCP scaffold has precise and controllable pore structure, while with the limitation of insufficient mechanical properties. In this study, we investigated the effect of sintering temperature on the mechanical properties of 3D-printed TCP scaffolds in detail, due to the important role of the sintering process on the mechanical properties of bioceramic scaffolds. The morphology, mass and volume shrinkage, porosity, mechanical properties and degradation property of the scaffold was studied. The results showed that the scaffold sintered at 1 150℃ had the maximum volume shrinkage, the minimum porosity and optimal mechanical strength, with the compressive strength of (6.52 ± 0.84) MPa and the compressive modulus of (100.08 ± 18.6) MPa, which could meet the requirements of human cancellous bone. In addition, the 1 150℃ sintered scaffold degraded most slowly in the acidic environment compared to the scaffolds sintered at the other temperatures, demonstrating its optimal mechanical stability over long-term implantation. The scaffold can support bone mesenchymal stem cells (BMSCs) adherence and rapid proliferation and has good biocompatibility. In summary, this paper optimizes the sintering process of 3D printed TCP scaffold and improves its mechanical properties, which lays a foundation for its application as a load-bearing bone.

Study on computer-aided deposition manufacturing of vascular tissue engineering scaffolds at low temperature / 生物医学工程学杂志

Since there is a clinical need for the tissue-engineered vascular graft (TEVG), fabricating the vascular scaffold individually appears to be necessary. In this work, we have developed the traditional tubular scaffold and branch vascular scaffold utilizing low-temperature deposition manufacturing (LDM) technology. Then different tubular scaffolds were fabricated by changing the processing parameters, and the morphological properties of the scaffolds were assessed. The scaffolds reproduced the structure of 3D vascular model accurately. Wall thickness of the scaffold increased with the increase of velocity ratio (V(L)/V(s)) and nozzle temperature, and both the micropore size and wall roughness were positively correlated with the nozzle temperature. However, the porosity was barely affected by the nozzle temperature. This approach, fabricating vascular scaffold with special structure and appearance features via LDM technology, is potential for the individual fabrication of vascular scaffold.

Inhibitory effects of saponins from Anemarrhena asphodeloides Bunge on the growth of vascular smooth muscle cells / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the effects of saponins from Anemarrhena asphodeloides Bunge (SAaB) (Botanical Name: Anemarrhena Asphodeloidis Rhizoma) on the growth of vascular smooth muscle cells (VSMCs).</p><p><b>METHODS</b>Cell proliferation was measured by a newly developed cell proliferation reagent, WST-1. Cell apoptosis was assayed by flow cytometry through detecting annexin V. Nitric oxide production was evaluated using confocal laser scanning microscopy with diaminofluorescein diacetate (DAF-2, DA). Cell aldose reductase (AR) activity, as well as the effect of Epalrestat and interleukin-1beta were also explored.</p><p><b>RESULTS</b>WST assay showed that cell proliferation induced by serum was significantly inhibited by SAaB (P<0.01). Flow cytometry analysis revealed that SAaB could enhance apoptotic rate of VSMCs (P<0.01). Nitric oxide production was significantly enhanced after administration of SAaB and interleukin-1beta. Moreover, AR activity of VSMCs was also remarkably inhibited by both SAaB and Epalrestat (P<0.01).</p><p><b>CONCLUSION</b>SAaB can inhibit proliferation and enhance apoptosis of VSMCs. It may protect vascular cells by inhibiting VSMC proliferation and augmenting apoptotic rate of VSMCs via NO-dependent pathway.</p>