11β-hydroxysteroid dehydrogenases-2 decreases the apoptosis of MC3T3/MLO-Y4 cells induced by glucocorticoids

The aim of the present study was to confirm the role of 11β-hydroxysteroid dehydrogenases type 2(11β-HSD-2) in steroid induced osteonecrosis of the femoral head(SANFH). We cultured mouse bone-like cells (MLO-Y4) and mouse osteoblast-like cells (MC3T3-E1). After overexpressed 11β-HSD-2 successfully, we induced cell apoptosis by dexamethasone (DXM). The level of cell apoptosis, the expression of Bcl-2 in MLO-Y4 cells and the expression of Fas and caspase8 in MC3T3-E1 cells were detected. Then, we constructed 11β-HSD-2 siRNA plasmid and represented it on MLO-Y4/MC3T3-E1 Cells, to down-regulate the 11β-HSD-2 expression. After that, we used dexamethasone to induce cell apoptosis. The level of cell apoptosis, the expression of Bcl-2 in MLO-Y4 cells and the expression of Fas and caspase8 in MC3T3-E1 cells were detected again. In the overexpression model of cells, we found that the amount of cell apoptosis, the expression of Fas and caspase8 in MC3T3-E1 cells are lower than that of control groups. The amount of cell apoptosis, the expression of Fas and caspase8 in MC3T3-E1 cells were more than before when we reduced the expression of 11β-HSD-2. In our study, we concluded that 11β-HSD-2 plays an important role in the development of bone or osteoblast cell apoptosis, and the decreased expression of 11β-HSD-2 may aggravate steroid induced bone/osteoblast cell apoptosis. •The relationship between the changes of 11β-HSD-2 and bone cell apoptosis was investigated.•The research used overexpression and siRNA technology to confirm the role of 11β-HSD-2 in SANFH.•This experiment was repeated three times, and the data is sufficient.