Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5504870 | Biochemical and Biophysical Research Communications | 2017 | 8 Pages |
Abstract
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.
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Biochemistry
Authors
Hao Zhang, Fuling Zhou, Zhenyu Pan, Xiangpeng Bu, Yaoqing Wang, Fan Chen,