The therapeutic method traditionally used in bone defect reconstruction is autologous bone grafting. The most common problems affecting this type of repair approach are bone absorption and donor trauma. The approach taken in this study overcomes these problems. Bone marrow stromal cells (BMSCs) provided the crucial seed cells. Fibrin biological scaffolds were formed by combining the BMSCs with concentrated growth factor (CGF). BMSCs were isolated from Wistar rat femurs; CGF was prepared from rat heart blood. Five repair groups were created for comparative purposes: (A) CGF + BMSCs; (B) CGF; (C) collagen + BMSCs; (D) collagen; (E) blank. After three months, the rats were sacrificed, and histopathology and three-dimensional CT images produced. Bone regeneration was significantly higher in the (A) CGF + BMSC group; osteogenesis was lower in the (B) CGF and (C) collagen + BMSC groups, at very similar levels; the (D) collagen and (E) blank groups scored the lowest results. Our research suggests that combining CGF with BMSCs leads to the formation of fibrin scaffolds that have a powerful effect on osteogenesis as well as a subsidiary angiogenic effect. SEM images of the CGF scaffolds cultured with BMSCs confirmed good CGF biocompatibility. The superior osteoinductive activity of the CGF + BMSC combination makes it an excellent biomaterial for bone regeneration.

Background: Our previous study proved thatSalvia miltiorrhizacould enhance fat graft survival by promoting adipogenesis. However, the effect of salvianolic acid B (Sal-B), the most abundant and bioactive water-soluble compound inSalvia miltiorrhiza, on fat graft survival has not yet been investigated.Objective: This study aims to investigate whether salvianolic acid B could improve fat graft survival and promote preadipocyte differentiation. The underlying mechanism has also been studied.Methods: In vivo, 0.2 ml of Coleman fat was transplanted into nude mice with salvianolic acid B. The grafts were evaluated by HE and IF at 2 and 4 weeks posttransplantation and by micro-CT at 4 weeks posttransplantation. In vitro, the adipogenesis and proliferative activities of salvianolic acid B were analyzed in cultured human adipose-derived stem cells (h-ADSCs) and 3T3-L1 cells to detect the mechanism by which salvianolic acid B affects graft survival.Results: In vivo, the weights and volumes of the fat grafts in the Sal-B-treated groups were significantly higher than those of the fat grafts in the control group. In addition, higher fat integrity and more viable adipocytes were observed in the Sal-B-treated groups. In vitro, salvianolic acid B showed the ability to promote 3T3-L1 and h-ADSC proliferation and adipogenesis.Conclusions: Our in vitro experiments demonstrated that salvianolic acid B can promote the proliferation of adipose stem cells and enhance the differentiation of adipose stem cells. Simultaneously, in vivo experiments showed that salvianolic acid B can improve the survival rate of fat transplantation. Therefore, our research shed light on the potential therapeutic usage of salvianolic acid B in improving the survival rate of fat transplantation.

Background: Autologous fat grafting is a common method for soft tissue defect repair. However, the high absorption rate of transplanted fat is currently a bottleneck in the process. Excessive inflammation is one of the main reasons for poor fat transplantation. Salvianolic acid B (Sal-B) is a herbal medicine that shows promise for improving the effectiveness of fat transplantation. Objective: The aim of this study was to improve fat graft survival by injecting Sal-B into fat grafts locally. Methods: In vivo, 0.2 mL of Coleman fat was transplanted into nude mice along with Sal-B. The grafts were evaluated by histologic analysis at 2, 4, and 12 weeks posttransplantation and by microcomputed tomography at 4 weeks posttransplantation. In vitro ribonucleic acid sequencing, cell proliferation assays, anti-inflammatory activity assays, molecular docking studies, and kinase activity assays were performed in RAW264.7 cells to detect the potential mechanism. Results: Sal-B significantly improved fat graft survival and attenuated adipose tissue fibrosis and inflammation. Sal-B also inhibited the polarization of M1 macrophages in fat grafts. In vitro, Sal-B inhibited the proliferation and activation of inflammatory pathways in RAW264.7 cells. In addition, Sal-B had an inhibitory effect on NF-κB (nuclear factor κ light polypeptide gene enhancer in B cells) signaling. This bioactivity of Sal-B may result from its selective binding to the kinase domain of the inhibitor of NF-κB kinase subunit β. Conclusions: Sal-B could serve as a promising agent for improving the effect of fat transplantation by inhibiting the polarization of M1 macrophages through NF-κB signaling.