PDF(Pubmed)
Abstract：
Osteoblasts and osteoclasts play a crucial role in the dynamically coupled balance during bone regeneration and remodeling. They complement and restrict each other in the human body. Decreased osteoblasts lead to insufficient bone formation or excessive formation of osteoclasts, leading to increased bone resorption, which will destroy the structure of the bone tissue. This will greatly increase the risk of diseases such as osteoporosis and nonunions caused by bone defects. Herein, gelatin and polycaprolactone were used as substrates, and biomaterial membranes with mesh and sandwich structures were constructed using the electrospinning technology. Naringenin was loaded into the shell, and vitamin K2 was loaded into the core layer of the nanofibrous membrane. The biocompatibility and osteogenic capacity of the membranes were assessed in vitro using mouse bone marrow mesenchymal stem cells (BMSCs). During osteoclast induction, the receptor activator of nuclear factor kappa-Β ligand (RANKL) was used to coculture RAW264.7 cells with various materials. The regulatory effect of various membranes on osteoclast growth was evaluated by detecting the expression levels of osteoclast-related genes and proteins in the cells. Subsequently, we constructed a model of a rat skull defect and implanted different membranes into the defect. Then, we evaluated the new bone formation in the defect using histological staining and micro-computed tomography after 4 and 8 weeks. The results of in vitro experiments confirmed that the incorporation of naringenin and vitamin K2 stimulated the expression of osteogenesis-related genes and the secretion of osteogenesis-related proteins. Simultaneously, the results showed that naringenin and vitamin K2 inhibited the formation and growth of osteoclasts. Therefore, naringenin and vitamin K2 have a synergistic effect in promoting bone growth and regulating osteoclast growth.
摘要：
成骨细胞和破骨细胞在骨再生和重建过程中的动态耦合平衡中起着至关重要的作用。它们在人体中相互补充和制约。成骨细胞减少导致骨形成不足或破骨细胞过度形成，导致骨吸收增加，会破坏骨组织的结构。这将大大增加由骨缺损引起的骨质疏松症和不愈合等疾病的风险。在这里，明胶和聚己内酯被用作底物，使用静电纺丝技术构建了具有网格和三明治结构的生物材料膜。Naringenin被装入外壳,并且维生素K2被加载到纳米纤维膜的核心层中。使用小鼠骨髓间充质干细胞（BMSCs）在体外评估膜的生物相容性和成骨能力。在破骨细胞诱导过程中，核因子κ-Β配体（RANKL）的受体激活剂用于将RAW264.7细胞与各种材料共培养。通过检测破骨细胞相关基因和蛋白质在细胞中的表达水平来评估各种膜对破骨细胞生长的调节作用。随后，我们构建了大鼠颅骨缺损模型，并将不同的膜植入缺损中。然后，我们在4周和8周后使用组织学染色和显微计算机断层扫描评估了缺损中的新骨形成。体外实验结果证实柚皮素和维生素K2的掺入刺激了成骨相关基因的表达和成骨相关蛋白的分泌。同时,结果表明，柚皮素和维生素K2抑制破骨细胞的形成和生长。因此,柚皮素和维生素K2在促进骨生长和调节破骨细胞生长方面具有协同作用。
