Abstract
Bone infection or osteomyelitis is usually a complication of inflammation-related traumatic bone injury. Selenium has been shown to have potential cytoprotective effects and the ability to reduce oxidative stress and apoptotic events in osteomyelitis, but the exact mechanism remains unclear. Here, we used LPS-induced apoptotic MC3T3-E1 cells and aimed to confirm selenium's protective effect on cell apoptosis as well as to investigate the underlying mechanisms of this role. Our investigation confirmed selenium-mediated inhibition of LPS-induced cell apoptosis and ROS accumulation in MC3T3-E1 cells. Upon selenium treatment, the bcl-2 levels were upregulated, while the levels of Bax and cyto-C were down-regulated. Furthermore, these effects were accompanied by the suppression of miR-155 and the phosphorylation of protein kinase B (Akt). A more in-depth study demonstrated that LY294002 (a specific inhibitor of PI3K), abolished the selenium-mediated cytoprotective effect of MC3T3-E1 cells against LPS-induced injury and down-regulation of miR-155. In general, these results demonstrated that selenium exerts a cytoprotective effect by attenuating cell apoptosis and oxidative damage via a PI3K/Akt/miR-155-dependent mechanism.
Highlights
Osteomyelitis is an infection of bones, typically characterized by bone destruction leading to bone resorption and dysfunction (Ian, 2013)
We examined the level of miR-155 and the activation of PI3K/Akt pathway in this process
Culturing MC3T3-E1 cells with 100 ng/ml of LPS enhanced their apoptosis to 28.5%, while culturing the cells with 200 ng/ml of LPS enhanced cell apoptosis to 36%
Summary
Osteomyelitis is an infection of bones, typically characterized by bone destruction leading to bone resorption and dysfunction (Ian, 2013). It can affect both children and adults, and usually develops in the limbs, especially the hip joints, the distal femur and proximal tibia, but any bone can be infected (Hatzenbuehler and Pulling, 2011). Previous studies found that LPS injection induced low turnover osteopenia and enhanced osteoblast apoptosis in TNFR1-/- mice (Ochi et al, 2010). The main objective of this study was to identify potential drugs that can inhibit LPS-mediated apoptosis in mouse osteoblast cell line
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
