Background
Recently, the antioxidant properties of the natural compound, selenomethionine (Se-Met), have been recognized. However, its effect on the osteogenic mineralization of the Wnt/β-Catenin pathway under conditions of oxidative stress and inflammation remain unclear.
Conclusion
Se-Met enhances antioxidant and anti-inflammatory responses in MC3T3-E1 cells via the Wnt/β-Catenin signaling pathway to promote osteogenesis. Thus, Se-Met plays a crucial role in the field of bone homeostasis, and presents an opportunity for the future development of novel drugs for treating osteoporosis and maintaining bone stability. However, further detailed preclinical animal studies are required to generate solid and reliable data to aid this development.
Methods
This study utilized tert-butyl hydroperoxide (TBHP) to simulate oxidative stress and inflammation. Se-Met was then subsequently used to inhibit these effects in vitro.
Results
TBHP induces oxidative stress and inflammatory responses by increasing the expression of reactive oxygen species and NLRP3, whereas decreasing the expression of GPX4, thereby inhibiting the viability of MC3T3-E1 cells. TBHP further promotes lipid peroxidation and damages the ultrastructure of mitochondria. Furthermore, TBHP inhibits the expression levels of β-Catenin, thereby reducing the activity of the Wnt pathway, which in turn suppresses the osteogenic differentiation and mineralization capacity. Importantly, Se-Met significantly alters the aforementioned responses to enhance expression levels of Wnt pathway-related proteins and improving the osteogenic differentiation and mineralization capacity of the cells.