TiO2nanotubes-MoS2/PDA-LL-37 exhibits efficient anti-bacterial activity and facilitates new bone formation under near-infrared laser irradiation.

Titanium dioxide (TiO2), as one of the titanium (Ti)-based implants, holds a promise for a variety of anti-bacterial application in medical research. In the current study, a functional molybdenum disulfide (MoS2)/polydopamine (PDA)-LL-37 coating on titanium dioxide (TiO2) implant was prepared. Anodic oxidation and hydrothermal treatment was given to prepare TiO2nanotubes-MoS2/PDA-LL-37 (T-M/P-L). Thein vitroosteogenic effect of T-M/P-L was evaluated by measuring mesenchymal stem cell (MSC) adhesion, proliferation, alkaline phosphatase (ALP) activity, extracellular matrix (ECM) mineralization, collagen secretion and osteoblast-specific messenger RNAs (mRNAs) expression. The determination on the anti-bacterial ability of T-M/P-L was followed. Furthermore, the ability of T-M/P-L to promote bone formationin vivowas evaluated. Near-infrared (NIR) laser irradiation exposure enabled the T-M/P-L coating-endowed Ti substrates to hold effective anti-bacterial ability. T-M/P-L promoted the adhesion and proliferation of MSCs. In addition, an increase was witnessed regarding the ALP activity, collagen secretion and ECM mineralization, along with the expression of runt-related transcription factor 2, ALP and osteocalcin in the presence of T-M/P-L. Additionally, T-M/P-L could stimulate endothelial cells to secrete vascular endothelial growth factor (VEGF) and promote capillary-like tubule formation. Upon NIR laser irradiation exposure, T-M/P-L not only exhibited efficientin vivoanti-bacterial activity but also facilitated new bone formation. Collectively, T-M/P-L had enhanced anti-bacterial and osteogenic activity under NIR laser irradiation.

Acacetin inhibits RANKL-induced osteoclastogenesis and LPS-induced bone loss by modulating NFATc1 transcription.

Osteolytic disorders are characterized by impaired bone volume and trabecular structure that leads to severe fragility fractures. Studies have shown that excessive osteoclast activity causes impaired bone microstructure, a sign of osteolytic diseases such as osteoporosis. Approaches of inhibiting osteoclastogenesis and bone resorption specifically could prevent osteoporosis and other osteolytic disorders. Acacetin is a potent molecule extracted from plants with anti-cancer and anti-inflammatory bioactivities. Here, we demonstrated, for the first time, that acacetin repressed osteoclastogenesis, formation of F-actin rings, bone resorption activity, and osteoclast-related gene expression in vitro through modulating ERK, P38, and NF-κB signaling pathways and preventing expression of NFATc1. Micro-CT and H & E staining results indicated that acacetin alleviated LPS-induced osteolysis in vivo. Overall, our findings suggested that acacetin could help to prevent osteoporosis and other osteoclast-related osteolytic disorders.